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levitra vs viagra Us Topics on Men's Health Barbara K. Hecht levitra vs viagra, Ph.D. Frederick Hecht levitra vs viagra, M.D. Medical Editors levitra vs viagra, MedicineNet.com August 19 levitra vs viagra, 2003 -- The Food and Drug Administration approved Levitra (vardenafil) levitra vs viagra, an oral medication to treat erectile dysfunction in men (impotence). This is the second oral product approved for the treatment of erectile dysfunction. (Sildenafil levitra vs viagra, better known as Viagra levitra vs viagra, was the first.) Erectile dysfunction affects millions of men in the United States. Levitra acts by relaxing muscles in the penis and blood vessels levitra vs viagra, allowing increased blood flow into the penis levitra vs viagra, which produces an erection. Levitra was evaluated in randomized levitra vs viagra, placebo-controlled trials inv levitra vs viagra.
levitra vs viagra Olving more than 2000 men with erectile dysfunction. In two of the trials men had erectile dysfunction associated with diabetes mellitus or following radical prostatectomy for prostate cancer. The drug's effectiveness was assessed using a sexual function questionnaire. In addition levitra vs viagra, patients were asked to report if they were able to achieve an erection adequate for intercourse and whether the erection was maintained to allow completion of intercourse. In all of the trials levitra vs viagra, Levitra improved patients' ability to achieve and maintain a penile erection. The recommended dose is 10 mg taken 1 hour before sexual activity. A higher dose of 20 mg is available for patients whose response to the 10 mg dose is not adequate. Two lower doses (2.5 mg and 5.0 mg) are also available and may be necessary for patients taking other medicines or having medical conditions that may decrease the body's ability to metabolize vardenafil (Levitra). Levitra should not be used more than once a day. Levitra should not be used with nitrates (such as nitroglycerin tablets or patches) or with alpha-blockers (medicines that may be used to treat benign prostatic hyperplasia and or high blood pressure such as tamsulosin levitra vs viagra, terazosin levitra vs viagra, doxazosin levitra vs viagra, and alfuzosin) because the combination of an alpha-blocker with Levitra may significantly lower the blood p.
levitra vs viagra Nts whose response to the 10 mg dose is not adequate. Two lower doses (2.5 mg and 5.0 mg) are also available and may be necessary for patients taking other medicines or having medical conditions that may decrease the body's ability to metabolize vardenafil (Levitra). Levitra should not be used more than once a day. Levitra should not be used with nitrates (such as nitroglycerin tablets or patches) or with alpha-blockers (medicines that may be used to treat benign prostatic hyperplasia and or high blood pressure such as tamsulosin levitra vs viagra, terazosin levitra vs viagra, doxazosin levitra vs viagra, and alfuzosin) because the combination of an alpha-blocker with Levitra may significantly lower the blood pr.
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998. All three are taken orally prior to planned sexual activity, acting to increase blood flow in the penis in response to sexual stimulation. However, there are important differences between the three, differences that could influence safety, specificity, duration of action, and ultimately, public acceptance within this class of drug. Giles Brindley and Drug Therapy for ED Modern drug therapy for ED was advanced enormously in 1983 when British physiologist Giles Brindley, Ph.D. dropped his trousers and demonstrated to a shocked AUA audience his phentolamine-induced erection. The drug Brindley injected into his penis was a non-specific vasodilator, an alpha-blocking agent, and the mechanism of action was clearly corporal smooth muscle relaxation. The effect that Brindley discovered, established the fundamentals for the later development of specific, safe, orally-effective drug therapies, ie, PDE-5 inhibitors. PDE Inhibition and Smooth Muscle Relaxation Phosphodiesterase (PDE) is an enzyme that causes breakdown of cyclic GMP, which is the direct intracellular mediator in the nitric oxide (nonadrenergic, noncholinergic) pathway. Discovery of this pathway led to a Nobel Prize in 1998 for the scientists responsible. The nitric oxide system causes relaxation of smooth muscle in blood vessel walls, ie, vasodilation, in various organ systems. The direct intracellular mediator of the nitric oxide pathway is cGMP. PDE catalyzes the degradation of cGMP. This pathway is active in numerous organ systems, and as of this writing, a number of different PDEs are known. The various PDEs di
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