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Viagra Vasodilator

viagra vasodilator

Vasodilation is the widening of blood vessels. The process is the opposite of vasoconstriction , which is the narrowing of blood vessels. When blood vessels dilate , the flow of blood is increased due to a decrease in vascular resistance and increase in cardiac output. Therefore, dilation of arterial blood vessels mainly the arterioles [ citation needed ] decreases blood pressure.

The response may be intrinsic due to local processes in the surrounding tissue or extrinsic due to hormones or the nervous system. In addition, the response may be localized to a specific organ depending on the metabolic needs of a particular tissue, as during strenuous exercise , or it may be systemic seen throughout the entire systemic circulation.

Endogenous substances and drugs that cause vasodilation are termed vasodilators. Such vasoactivity is necessary for homeostasis keeping the body running normally.

The primary function of vasodilation is to increase blood flow in the body to tissues that need it most. This is often in response to a localized need for oxygen but can occur when the tissue in question is not receiving enough glucose , lipids , or other nutrients. Localized tissues have multiple ways to increase blood flow, including releasing vasodilators, primarily adenosine , into the local interstitial fluid , which diffuses to capillary beds, provoking local vasodilation.

This latter hypothesis is posited due to the presence of precapillary sphincters in capillary beds. These approaches to the mechanism of vasodilation are not mutually exclusive. Vasodilation directly affects the relationship between mean arterial pressure , cardiac output , and total peripheral resistance TPR. Vasodilation occurs in the time phase of cardiac systole , whereas vasoconstriction follows in the opposite time phase of cardiac diastole. Cardiac output blood flow measured in volume per unit time is computed by multiplying the heart rate in beats per minute and the stroke volume the volume of blood ejected during ventricular systole.

TPR depends on several factors, including the length of the vessel, the viscosity of blood determined by hematocrit and the diameter of the blood vessel. The latter is the most important variable in determining resistance, with the TPR changing by the fourth power of the.

An increase in either of these physiological components cardiac output or TPR causes a rise in the mean arterial pressure. Vasodilation works to decrease TPR and blood pressure through relaxation of smooth muscle cells in the tunica media layer of large arteries and smaller arterioles.

Vasodilation occurs in superficial blood vessels of warm-blooded animals when their ambient environment is hot; this process diverts the flow of heated blood to the skin of the animal, where heat can be more easily released to the atmosphere. The opposite physiological process is vasoconstriction. These processes are naturally modulated by local paracrine agents from endothelial cells e.

Vasodilation is the result of relaxation in smooth muscle surrounding the blood vessels. This relaxation, in turn, relies on removing the stimulus for contraction, which depends on intracellular calcium ion concentrations and is tightly linked with phosphorylation of the light chain of the contractile protein myosin. Thus, vasodilation works mainly either by lowering intracellular calcium concentration or by dephosphorylation really substitution of ATP for ADP of myosin.

Dephosphorylation by myosin light-chain phosphatase and induction of calcium symporters and antiporters that pump calcium ions out of the intracellular compartment both contribute to smooth muscle cell relaxation and therefore vasodilation. This is accomplished through reuptake of ions into the sarcoplasmic reticulum via exchangers and expulsion across the plasma membrane. The specific mechanisms to accomplish these effects vary from vasodilator to vasodilator.

PDE5 inhibitors and potassium channel openers can also have similar results. Compounds that mediate the above mechanisms may be grouped as endogenous and exogenous. The vasodilating action of activation of beta-2 receptors such as by adrenaline appears to be endothelium -independent. Although it is recognized that the sympathetic nervous system plays an expendable role in vasodilation, it is only one of the mechanisms by which vasodilation can be accomplished.

The spinal cord has both vasodilation and vasoconstriction nerves. The neurons that control vascular vasodilation originate in the hypothalamus. However, it has been shown that knocking out this sympathetic stimulation plays little or no role in whether skeletal muscle is able to receive sufficient oxygen even at high levels of exertion, so it is believed that this particular method of vasodilation is of little importance to human physiology.

In cases of emotional distress, this system may activate, resulting in fainting due to decreased blood pressure from vasodilation, which is referred to as vasovagal syncope. Cold-induced vasodilation CIVD occurs after cold exposure, possibly to reduce the risk of injury. It can take place in several locations in the human body but is observed most often in the extremities.

The fingers are especially common because they are exposed most often. When the fingers are exposed to cold, vasoconstriction occurs first to reduce heat loss, resulting in strong cooling of the fingers. Approximately five to ten minutes after the start of the cold exposure of the hand, the blood vessels in the finger tips will suddenly vasodilate.

This is probably caused by a sudden decrease in the release of neurotransmitters from the sympathetic nerves to the muscular coat of the arteriovenous anastomoses due to local cold. The CIVD increases blood flow and subsequently the temperature of the fingers. This can be painful and is sometimes known as the ' hot aches ' which can be painful enough to bring on vomiting.

A new phase of vasoconstriction follows the vasodilation, after which the process repeats itself. This is called the Hunting reaction. Experiments have shown that three other vascular responses to immersion of the finger in cold water are possible: However, the vast majority of responses can be classified as the Hunting reaction. Vasodilators are used to treat conditions such as hypertension , wherein the patient has an abnormally high blood pressure, as well as angina , congestive heart failure , and erectile dysfunction , and where maintaining a lower blood pressure reduces the patient's risk of developing other cardiac problems.

Some phosphodiesterase inhibitors such as sildenafil , vardenafil and tadalafil , work to increase blood flow in the penis through vasodilation. They may also be used to treat pulmonary arterial hypertension PAH. From Wikipedia, the free encyclopedia. This article is in a list format that may be better presented using prose. You can help by converting this article to prose, if appropriate. Editing help is available. This article needs more medical references for verification or relies too heavily on primary sources.

Please review the contents of the article and add the appropriate references if you can. Unsourced or poorly sourced material may be challenged and removed. Retrieved 13 January American Journal of Physiology. Heart and Circulatory Physiology.

Textbook of Medical Physiology Book 11th ed. Journal of applied physiology Bethesda, Md. Advances in Physiology Education. A Cellular And Molecular Approaoch. Dale; Ritter, James M. Clinical Pharmacology and Therapeutics. European Journal of Applied Physiology. Emollients Cicatrizants Antipruritics Antipsoriatics Medicated dressings.

Anticancer agents Antimetabolites Alkylating Spindle poisons Antineoplastic Topoisomerase inhibitors.

Decongestants Bronchodilators Cough medicines H 1 antagonists. Antidotes Contrast media Radiopharmaceuticals Dressings Senotherapeutics. Vasodilators used in cardiac diseases C01D. Nonsympatholytic vasodilatory antihypertensives C Niacin Nicotinyl alcohol Inositol nicotinate Ciclonicate. Pentifylline Xantinol nicotinate Pentoxifylline Etofylline nicotinate. Physiology of the cardiovascular system. Central venous Right atrial ventricular pulmonary artery wedge Left atrial ventricular Aortic.

Compliance Vascular resistance Pulse Perfusion. Pulse pressure Systolic Diastolic Mean arterial pressure Jugular venous pressure Portal venous pressure.

Baroreflex Kinin—kallikrein system Renin—angiotensin system Vasoconstrictors Vasodilators Autoregulation Myogenic mechanism Tubuloglomerular feedback Cerebral autoregulation Paraganglia Aortic body Carotid body Glomus cell. Retrieved from " https: All articles with unsourced statements Articles with unsourced statements from January Articles needing cleanup from June All pages needing cleanup Articles with sections that need to be turned into prose from June Articles needing additional medical references from September All articles needing additional references Articles requiring reliable medical sources Wikipedia articles with GND identifiers Use dmy dates from March Views Read Edit View history.

This page was last edited on 17 February , at By using this site, you agree to the Terms of Use and Privacy Policy. Hyperpolarization -mediated Calcium channel blocker. Changes in the resting membrane potential of the cell affects the level of intracellular calcium through modulation of voltage-sensitive calcium channels in the plasma membrane.

Adrenergic stimulation results in elevated levels of cAMP and protein kinase A , which results in increasing calcium removal from the cytoplasm. Through stimulation of protein kinase G. NO receptor on endothelium. A 1 , A 2a and A 2b adenosine receptors. Scholia has a topic profile for Vasodilation. NO arterioles and venules Nitroprusside. Blood flow Compliance Vascular resistance Pulse Perfusion.

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Viagra vasodilator

Dephosphorylation by myosin light-chain phosphatase and induction of calcium symporters and antiporters that pump calcium ions out of the intracellular compartment both contribute to smooth muscle cell relaxation and therefore vasodilation. This is accomplished through reuptake of ions into the sarcoplasmic reticulum via exchangers and expulsion across the plasma membrane. The specific mechanisms to accomplish these effects vary from vasodilator to vasodilator.

PDE5 inhibitors and potassium channel openers can also have similar results. Compounds that mediate the above mechanisms may be grouped as endogenous and exogenous. The vasodilating action of activation of beta-2 receptors such as by adrenaline appears to be endothelium -independent. Although it is recognized that the sympathetic nervous system plays an expendable role in vasodilation, it is only one of the mechanisms by which vasodilation can be accomplished. The spinal cord has both vasodilation and vasoconstriction nerves.

The neurons that control vascular vasodilation originate in the hypothalamus. However, it has been shown that knocking out this sympathetic stimulation plays little or no role in whether skeletal muscle is able to receive sufficient oxygen even at high levels of exertion, so it is believed that this particular method of vasodilation is of little importance to human physiology. In cases of emotional distress, this system may activate, resulting in fainting due to decreased blood pressure from vasodilation, which is referred to as vasovagal syncope.

Cold-induced vasodilation CIVD occurs after cold exposure, possibly to reduce the risk of injury. It can take place in several locations in the human body but is observed most often in the extremities. The fingers are especially common because they are exposed most often.

When the fingers are exposed to cold, vasoconstriction occurs first to reduce heat loss, resulting in strong cooling of the fingers. Approximately five to ten minutes after the start of the cold exposure of the hand, the blood vessels in the finger tips will suddenly vasodilate. This is probably caused by a sudden decrease in the release of neurotransmitters from the sympathetic nerves to the muscular coat of the arteriovenous anastomoses due to local cold.

The CIVD increases blood flow and subsequently the temperature of the fingers. This can be painful and is sometimes known as the ' hot aches ' which can be painful enough to bring on vomiting. A new phase of vasoconstriction follows the vasodilation, after which the process repeats itself. This is called the Hunting reaction. Experiments have shown that three other vascular responses to immersion of the finger in cold water are possible: However, the vast majority of responses can be classified as the Hunting reaction.

Vasodilators are used to treat conditions such as hypertension , wherein the patient has an abnormally high blood pressure, as well as angina , congestive heart failure , and erectile dysfunction , and where maintaining a lower blood pressure reduces the patient's risk of developing other cardiac problems. Some phosphodiesterase inhibitors such as sildenafil , vardenafil and tadalafil , work to increase blood flow in the penis through vasodilation.

They may also be used to treat pulmonary arterial hypertension PAH. From Wikipedia, the free encyclopedia. This article is in a list format that may be better presented using prose. You can help by converting this article to prose, if appropriate. Editing help is available. This article needs more medical references for verification or relies too heavily on primary sources. Please review the contents of the article and add the appropriate references if you can.

Unsourced or poorly sourced material may be challenged and removed. Retrieved 13 January American Journal of Physiology. Heart and Circulatory Physiology. Textbook of Medical Physiology Book 11th ed. Journal of applied physiology Bethesda, Md. Advances in Physiology Education. A Cellular And Molecular Approaoch. Dale; Ritter, James M. Clinical Pharmacology and Therapeutics. European Journal of Applied Physiology.

Emollients Cicatrizants Antipruritics Antipsoriatics Medicated dressings. Anticancer agents Antimetabolites Alkylating Spindle poisons Antineoplastic Topoisomerase inhibitors. Decongestants Bronchodilators Cough medicines H 1 antagonists. Antidotes Contrast media Radiopharmaceuticals Dressings Senotherapeutics.

Vasodilators used in cardiac diseases C01D. In some of the cases, medical conditions and other factors were reported that may have also played a role in the otologic adverse events. In many cases, medical follow-up information was limited. It is not possible to determine whether these reported events are related directly to the use of Viagra, to the patient's underlying risk factors for hearing loss, a combination of these factors, or to other factors [ see Warnings and Precautions 5.

Non-arteritic anterior ischemic optic neuropathy NAION , a cause of decreased vision including permanent loss of vision, has been reported rarely post-marketing in temporal association with the use of phosphodiesterase type 5 PDE5 inhibitors, including Viagra. Most, but not all, of these patients had underlying anatomic or vascular risk factors for developing NAION, including but not necessarily limited to: Administration of Viagra with nitric oxide donors such as organic nitrates or organic nitrites in any form is contraindicated.

Use caution when co-administering alpha-blockers with Viagra because of potential additive blood pressure-lowering effects. When Viagra is co-administered with an alpha-blocker, patients should be stable on alpha-blocker therapy prior to initiating Viagra treatment and Viagra should be initiated at the lowest dose [ see Dosage and Administration 2.

When Viagra mg was co-administered with amlodipine 5 mg or 10 mg to hypertensive patients, the mean additional reduction on supine blood pressure was 8 mmHg systolic and 7 mmHg diastolic [ see Warnings and Precautions 5. Co-administration of ritonavir, a strong CYP3A4 inhibitor, greatly increased the systemic exposure of sildenafil fold increase in AUC.

It is therefore recommended not to exceed a maximum single dose of 25 mg of Viagra in a 48 hour period [ see Dosage and Administration 2. Stronger CYP3A4 inhibitors such as ketoconazole or itraconazole could be expected to have greater effects than seen with saquinavir. A starting dose of 25 mg of Viagra should be considered in patients taking erythromycin or strong CYP3A4 inhibitors such as saquinavir, ketoconazole, itraconazole [ see Dosage and Administration 2.

In a drug-drug interaction study sildenafil 50 mg given with alcohol 0. There are no data with the use of Viagra in pregnant women to inform any drug-associated risks for adverse developmental outcomes. Limited data indicate that sildenafil and its active metabolite are present in human milk.

There is no information on the effects on the breastfed child, or the effects on milk production. Viagra is not indicated for use in pediatric patients. Safety and effectiveness have not been established in pediatric patients. However, since higher plasma levels may increase the incidence of adverse reactions, a starting dose of 25 mg should be considered in older subjects due to the higher systemic exposure [ see Dosage and Administration 2.

A starting dose of 25 mg should be considered in patients with severe renal impairment [ see Dosage and Administration 2. The pharmacokinetics of sildenafil in patients with severely impaired hepatic function Child-Pugh Class C have not been studied.

A starting dose of 25 mg should be considered in patients with any degree of hepatic impairment [ see Dosage and Administration 2. In studies with healthy volunteers of single doses up to mg, adverse reactions were similar to those seen at lower doses but incidence rates and severities were increased.

In cases of overdose, standard supportive measures should be adopted as required. Renal dialysis is not expected to accelerate clearance as sildenafil is highly bound to plasma proteins and it is not eliminated in the urine.

Viagra sildenafil citrate , an oral therapy for erectile dysfunction, is the citrate salt of sildenafil, a selective inhibitor of cyclic guanosine monophosphate cGMP -specific phosphodiesterase type 5 PDE5. Sildenafil citrate is designated chemically as 1-[[3- 6,7-dihydromethyloxopropyl-1 H -pyrazolo[4,3- d ]pyrimidinyl ethoxyphenyl]sulfonyl]methylpiperazine citrate and has the following structural formula:.

Sildenafil citrate is a white to off-white crystalline powder with a solubility of 3. Viagra is formulated as blue, film-coated rounded-diamond-shaped tablets equivalent to 25 mg, 50 mg and mg of sildenafil for oral administration. In addition to the active ingredient, sildenafil citrate, each tablet contains the following inactive ingredients: The physiologic mechanism of erection of the penis involves release of nitric oxide NO in the corpus cavernosum during sexual stimulation.

NO then activates the enzyme guanylate cyclase, which results in increased levels of cyclic guanosine monophosphate cGMP , producing smooth muscle relaxation in the corpus cavernosum and allowing inflow of blood.

Sildenafil enhances the effect of NO by inhibiting phosphodiesterase type 5 PDE5 , which is responsible for degradation of cGMP in the corpus cavernosum. Sildenafil has no direct relaxant effect on isolated human corpus cavernosum. When sexual stimulation causes local release of NO, inhibition of PDE5 by sildenafil causes increased levels of cGMP in the corpus cavernosum, resulting in smooth muscle relaxation and inflow of blood to the corpus cavernosum.

Sildenafil at recommended doses has no effect in the absence of sexual stimulation. Studies in vitro have shown that sildenafil is selective for PDE5. PDE3 is involved in control of cardiac contractility. Sildenafil is only about fold as potent for PDE5 compared to PDE6, an enzyme found in the retina which is involved in the phototransduction pathway of the retina. This lower selectivity is thought to be the basis for abnormalities related to color vision [ see Clinical Pharmacology In addition to human corpus cavernosum smooth muscle, PDE5 is also found in other tissues including platelets, vascular and visceral smooth muscle, and skeletal muscle, brain, heart, liver, kidney, lung, pancreas, prostate, bladder, testis, and seminal vesicle.

The inhibition of PDE5 in some of these tissues by sildenafil may be the basis for the enhanced platelet antiaggregatory activity of NO observed in vitro , an inhibition of platelet thrombus formation in vivo and peripheral arterial-venous dilatation in vivo. Effects of Viagra on Erectile Response: Most studies assessed the efficacy of Viagra approximately 60 minutes post dose. The time course of effect was examined in one study, showing an effect for up to 4 hours but the response was diminished compared to 2 hours.

Effects of Viagra on Blood Pressure: The decrease in sitting blood pressure was most notable approximately 1—2 hours after dosing, and was not different than placebo at 8 hours. Similar effects on blood pressure were noted with 25 mg, 50 mg and mg of Viagra, therefore the effects are not related to dose or plasma levels within this dosage range. Larger effects were recorded among patients receiving concomitant nitrates [ see Contraindications 4. In the following patients: Although plasma levels of sildenafil at 24 hours post dose are much lower than at peak concentration, it is unknown whether nitrates can be safely co-administered at this time point [ see Contraindications 4.

Three double-blind, placebo-controlled, randomized, two-way crossover studies were conducted to assess the interaction of Viagra with doxazosin, an alpha-adrenergic blocking agent. In the first study, a single oral dose of Viagra mg or matching placebo was administered in a 2-period crossover design to 4 generally healthy males with benign prostatic hyperplasia BPH. Following at least 14 consecutive daily doses of doxazosin, Viagra mg or matching placebo was administered simultaneously with doxazosin.

Following a review of the data from these first 4 subjects details provided below , the Viagra dose was reduced to 25 mg. Thereafter, 17 subjects were treated with Viagra 25 mg or matching placebo in combination with doxazosin 4 mg 15 subjects or doxazosin 8 mg 2 subjects.

The mean subject age was The mean profiles of the change from baseline in standing systolic blood pressure in subjects treated with doxazosin in combination with 25 mg Viagra or matching placebo are shown in Figure 2. Blood pressure was measured immediately pre-dose and at 15, 30, 45 minutes, and 1, 1. No severe adverse events potentially related to blood pressure effects were reported in this group.

Of the four subjects who received Viagra mg in the first part of this study, a severe adverse event related to blood pressure effect was reported in one patient postural hypotension that began 35 minutes after dosing with Viagra with symptoms lasting for 8 hours , and mild adverse events potentially related to blood pressure effects were reported in two others dizziness, headache and fatigue at 1 hour after dosing; and dizziness, lightheadedness and nausea at 4 hours after dosing.

There were no reports of syncope among these patients. For these four subjects, the placebo-subtracted mean maximum decreases from baseline in supine and standing systolic blood pressures were Both of these subjects were protocol violators, one due to a low baseline standing SBP, and the other due to baseline orthostatic hypotension. In the second study, a single oral dose of Viagra 50 mg or matching placebo was administered in a 2-period crossover design to 20 generally healthy males with BPH.

Following at least 14 consecutive days of doxazosin, Viagra 50 mg or matching placebo was administered simultaneously with doxazosin 4 mg 17 subjects or with doxazosin 8 mg 3 subjects. The mean subject age in this study was Twenty subjects received Viagra 50 mg, but only 19 subjects received matching placebo. One patient discontinued the study prematurely due to an adverse event of hypotension following dosing with Viagra 50 mg.

This patient had been taking minoxidil, a potent vasodilator, during the study. The mean profiles of the change from baseline in standing systolic blood pressure in subjects treated with doxazosin in combination with 50 mg Viagra or matching placebo are shown in Figure 3. Blood pressure was measured after administration of Viagra at the same times as those specified for the first doxazosin study. In these two subjects, hypotension was reported as a moderately severe adverse event, beginning at approximately 1 hour after administration of Viagra 50 mg and resolving after approximately 7.

There were no severe adverse events potentially related to blood pressure and no episodes of syncope reported in this study. In the third study, a single oral dose of Viagra mg or matching placebo was administered in a 3-period crossover design to 20 generally healthy males with BPH.

In dose period 1, subjects were administered open-label doxazosin and a single dose of Viagra 50 mg simultaneously, after at least 14 consecutive days of doxazosin. If a subject did not successfully complete this first dosing period, he was discontinued from the study.

Subjects who had successfully completed the previous doxazosin interaction study using Viagra 50 mg , including no significant hemodynamic adverse events, were allowed to skip dose period 1. Treatment with doxazosin continued for at least 7 days after dose period 1.

Thereafter, Viagra mg or matching placebo was administered simultaneously with doxazosin 4 mg 14 subjects or doxazosin 8 mg 6 subjects in standard crossover fashion. Twenty-five subjects were screened. Two were discontinued after study period 1: Of the twenty subjects who were ultimately assigned to treatment, a total of 13 subjects successfully completed dose period 1, and seven had successfully completed the previous doxazosin study using Viagra 50 mg.

The mean profiles of the change from baseline in standing systolic blood pressure in subjects treated with doxazosin in combination with mg Viagra or matching placebo are shown in Figure 4. Blood pressure was measured after administration of Viagra at the same times as those specified for the previous doxazosin studies. All three were taking Viagra mg, and all three reported mild adverse events at the time of reductions in standing SBP, including vasodilation and lightheadedness.

While there were no severe adverse events potentially related to blood pressure reported in this study, one subject reported moderate vasodilatation after both Viagra 50 mg and mg. There were no episodes of syncope reported in this study. When Viagra mg oral was co-administered with amlodipine, 5 mg or 10 mg oral, to hypertensive patients, the mean additional reduction on supine blood pressure was 8 mmHg systolic and 7 mmHg diastolic.

Viagra 50 mg did not potentiate the hypotensive effect of alcohol 0. The maximum observed decrease in systolic blood pressure was The maximum observed decrease in diastolic blood pressure was There were no reports of postural dizziness or orthostatic hypotension.

The maximum recommended dose of mg sildenafil was not evaluated in this study [ see Drug Interactions 7. Effects of Viagra on Cardiac Parameters: Single oral doses of sildenafil up to mg produced no clinically relevant changes in the ECGs of normal male volunteers. Studies have produced relevant data on the effects of Viagra on cardiac output.

In one small, open-label, uncontrolled, pilot study, eight patients with stable ischemic heart disease underwent Swan-Ganz catheterization. A total dose of 40 mg sildenafil was administered by four intravenous infusions. Even though this total dosage produced plasma sildenafil concentrations which were approximately 2 to 5 times higher than the mean maximum plasma concentrations following a single oral dose of mg in healthy male volunteers, the hemodynamic response to exercise was preserved in these patients.

In a double-blind study, patients with erectile dysfunction and chronic stable angina limited by exercise, not receiving chronic oral nitrates, were randomized to a single dose of placebo or Viagra mg 1 hour prior to exercise testing.

The primary endpoint was time to limiting angina in the evaluable cohort. The mean times adjusted for baseline to onset of limiting angina were These results demonstrated that the effect of Viagra on the primary endpoint was statistically non-inferior to placebo. Effects of Viagra on Vision: At single oral doses of mg and mg, transient dose-related impairment of color discrimination was detected using the Farnsworth-Munsell hue test, with peak effects near the time of peak plasma levels.

This finding is consistent with the inhibition of PDE6, which is involved in phototransduction in the retina. An evaluation of visual function at doses up to twice the maximum recommended dose revealed no effects of Viagra on visual acuity, intraocular pressure, or pupillometry. Effects of Viagra on Sperm: There was no effect on sperm motility or morphology after single mg oral doses of Viagra in healthy volunteers. The pharmacokinetics of sildenafil are dose-proportional over the recommended dose range.

It is eliminated predominantly by hepatic metabolism mainly CYP3A4 and is converted to an active metabolite with properties similar to the parent, sildenafil. Both sildenafil and the metabolite have terminal half lives of about 4 hours. Mean sildenafil plasma concentrations measured after the administration of a single oral dose of mg to healthy male volunteers is depicted below:.

Viagra is rapidly absorbed. Maximum observed plasma concentrations are reached within 30 to minutes median 60 minutes of oral dosing in the fasted state.

The mean steady state volume of distribution Vss for sildenafil is L, indicating distribution into the tissues.

Protein binding is independent of total drug concentrations. Based upon measurements of sildenafil in semen of healthy volunteers 90 minutes after dosing, less than 0. The major circulating metabolite results from N-desmethylation of sildenafil, and is itself further metabolized. Similar values for pharmacokinetic parameters were seen in normal volunteers and in the patient population, using a population pharmacokinetic approach.

The pharmacokinetics of sildenafil in patients with severely impaired hepatic function Child-Pugh Class C have not been studied [ see Dosage and Administration 2. A starting oral dose of 25 mg should be considered in those patients [ see Dosage and Administration 2.

Therefore, inhibitors of these isoenzymes may reduce sildenafil clearance and inducers of these isoenzymes may increase sildenafil clearance. The concomitant use of erythromycin or strong CYP3A4 inhibitors e. Viagra had no effect on saquinavir pharmacokinetics. A stronger CYP3A4 inhibitor such as ketoconazole or itraconazole could be expected to have greater effect than that seen with saquinavir. Population pharmacokinetic data from patients in clinical trials also indicated a reduction in sildenafil clearance when it was co-administered with CYP3A4 inhibitors such as ketoconazole, erythromycin, or cimetidine [ see Dosage and Administration 2.

This is consistent with ritonavir's marked effects on a broad range of P substrates. Viagra had no effect on ritonavir pharmacokinetics [ see Dosage and Administration 2. Although the interaction between other protease inhibitors and sildenafil has not been studied, their concomitant use is expected to increase sildenafil levels.

In a study of healthy male volunteers, co-administration of sildenafil at steady state 80 mg t. Concomitant administration of strong CYP3A4 inducers, such as rifampin, is expected to cause greater decreases in plasma levels of sildenafil.

In healthy male volunteers, there was no evidence of a clinically significant effect of azithromycin mg daily for 3 days on the systemic exposure of sildenafil or its major circulating metabolite.

Pharmacokinetic data from patients in clinical trials showed no effect on sildenafil pharmacokinetics of CYP2C9 inhibitors such as tolbutamide, warfarin , CYP2D6 inhibitors such as selective serotonin reuptake inhibitors, tricyclic antidepressants , thiazide and related diuretics, ACE inhibitors, and calcium channel blockers. These effects on the metabolite are not expected to be of clinical consequence. No significant interactions were shown with tolbutamide mg or warfarin 40 mg , both of which are metabolized by CYP2C9.

In a study of healthy male volunteers, sildenafil mg did not affect the steady state pharmacokinetics of the HIV protease inhibitors, saquinavir and ritonavir, both of which are CYP3A4 substrates. Sildenafil at steady state, at a dose not approved for the treatment of erectile dysfunction 80 mg t. Sildenafil was not carcinogenic when administered to rats for 24 months at a dose resulting in total systemic drug exposure AUCs for unbound sildenafil and its major metabolite of and times, for male and female rats, respectively, the exposures observed in human males given the Maximum Recommended Human Dose MRHD of mg.

Sildenafil was negative in in vitro bacterial and Chinese hamster ovary cell assays to detect mutagenicity, and in vitro human lymphocytes and in vivo mouse micronucleus assays to detect clastogenicity.

In clinical studies, Viagra was assessed for its effect on the ability of men with erectile dysfunction ED to engage in sexual activity and in many cases specifically on the ability to achieve and maintain an erection sufficient for satisfactory sexual activity. Viagra was evaluated primarily at doses of 25 mg, 50 mg and mg in 21 randomized, double-blind, placebo-controlled trials of up to 6 months in duration, using a variety of study designs fixed dose, titration, parallel, crossover.

Viagra was administered to more than 3, patients aged 19 to 87 years, with ED of various etiologies organic, psychogenic, mixed with a mean duration of 5 years. Viagra demonstrated statistically significant improvement compared to placebo in all 21 studies. The studies that established benefit demonstrated improvements in success rates for sexual intercourse compared with placebo. Efficacy Endpoints in Controlled Clinical Studies. The effectiveness of Viagra was evaluated in most studies using several assessment instruments.

The primary measure in the principal studies was a sexual function questionnaire the International Index of Erectile Function - IIEF administered during a 4-week treatment-free run-in period, at baseline, at follow-up visits, and at the end of double-blind, placebo-controlled, at-home treatment. Two of the questions from the IIEF served as primary study endpoints; categorical responses were elicited to questions about 1 the ability to achieve erections sufficient for sexual intercourse and 2 the maintenance of erections after penetration.

The patient addressed both questions at the final visit for the last 4 weeks of the study. The possible categorical responses to these questions were 0 no attempted intercourse, 1 never or almost never, 2 a few times, 3 sometimes, 4 most times, and 5 almost always or always. Also collected as part of the IIEF was information about other aspects of sexual function, including information on erectile function, orgasm, desire, satisfaction with intercourse, and overall sexual satisfaction.

Sexual function data were also recorded by patients in a daily diary. In addition, patients were asked a global efficacy question and an optional partner questionnaire was administered. Efficacy Results from Controlled Clinical Studies.

The effect on one of the major end points, maintenance of erections after penetration, is shown in Figure 6, for the pooled results of 5 fixed-dose, dose-response studies of greater than one month duration, showing response according to baseline function.

Results with all doses have been pooled, but scores showed greater improvement at the 50 and mg doses than at 25 mg. The pattern of responses was similar for the other principal question, the ability to achieve an erection sufficient for intercourse.

Viagra vasodilator

Tell your healthcare provider about all the medicines you take 1including prescription and over-the-counter medicines, vitamins, and herbal supplements. The spinal cord has both vasodilation and vasoconstriction nerves. In clinical studies, Viagra was sildenafilo actavis for its effect on the ability of men with erectile dysfunction ED to engage in sexual activity and in many cases specifically on the ability to achieve and maintain an erection sufficient for satisfactory sexual activity. Editing help is available. Of the twenty subjects who were ultimately assigned to treatment, a total of 13 subjects successfully completed dose period 1, and seven had successfully completed the previous doxazosin study using Viagra 50 mg. In the second study, a single oral dose of Viagra 50 mg or matching placebo was administered in a 2-period crossover design to 20 generally healthy males with BPH. Viagra has systemic vasodilatory properties and may further lower blood pressure in patients taking anti-hypertensive medications, viagra vasodilator.

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