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Cellular Effects of Sildenafil (Viagra)

Erectile Dysfunction (ED), also known as impotence, affects a large segment of the male population over 40 years of age. ED results from impaired relaxation of the smooth muscle cells in the corpus cavernosum and in the penile arteries. Upon sexual stimulation, the increase in parasympathetic activity results in dilation of the cavernosal arteries and increased blood flow. At the same time, relaxation of the trabecular smooth muscle increases the compliance of the cavernous spaces, which facilitates blood flow. The increase in blood volume and the compression of the relaxed trabecular muscle against the tunica albuginea results in collapse of the venules and obstruction of venous outflow...

Cellular Effects of Sildenafil (Viagra)

Pathway Summary

Erectile Dysfunction (ED), also known as impotence, affects a large segment of the male population over 40 years of age. ED results from impaired relaxation of the smooth muscle cells in the corpus cavernosum and in the penile arteries. Upon sexual stimulation, the increase in parasympathetic activity results in dilation of the cavernosal arteries and increased blood flow. At the same time, relaxation of the trabecular smooth muscle increases the compliance of the cavernous spaces, which facilitates blood flow. The increase in blood volume and the compression of the relaxed trabecular muscle against the tunica albuginea results in collapse of the venules and obstruction of venous outflow. Once this occurs, blood ceases to flow through the cavernosal arteries, and a rigid erection occurs. The major mediator of relaxation of the smooth muscle cells in the cavernosal arteries and the trabecular muscle is nitric oxide (NO).Upon sexual stimulation, NO is produced by eNOS in the endothelium of the penile and cavernosal arteries, and by NNOS in the non-adrenergic/non-cholinergic nerve terminals (NANC) that densely innervate the corpus cavernosum. Sexual stimulation also enables the release of neurotransmitters, hormones and ANP, which along with NO regulate the smooth muscle tone by altering cellular Ca2+ levels. NO activates soluble guanylate cyclase (sGC) whereas ANP activates membrane-bound (mGC), which both cause an increase in cGMP levels. Neurotransmitters and hormones activate G-proteins such as G-αs, and bicarbonate ions activate mAC and sAC to increase cAMP levels. G-proteins also stimulate PLC which results in IP3 production. IP3, upon IP3R activation, modulates release of Ca2+ from intracellular calcium stores. These compounds (cAMP, cGMP and Ca2+) cause smooth muscle relaxation through a variety of mechanisms, including protein phosphorylation and gating of ion channels.Smooth muscle tone is regulated by cellular Ca2+, which activates MLCK and results in MLC phosphorylation and muscle contraction. Activation of MLC phosphatase reverses this process to activate actin-myosin cross bridging and smooth muscle relaxation of corpus cavernosum resulting in penile erection. The levels of cGMP and cAMP in the cell reflect the dynamic balance between muscle relaxation and contraction. cAMP activates MLCK activity by increasing Ca2+ influx through CNG and CaCn activation, whereas cAMP-dependent PKA activation inhibits MLCK. Levels of cGMP reflect a balance between production of NO by NOS and degradation of cGMP by cyclic nucleotide phosphodiesterases (PDE). cGMP causes smooth muscle relaxation through a variety of mechanisms that includes phosphorylation and opening of KCn, activation of PKG, and interactions with PDE. Opening of potassium channels leads to hyperpolarization, closure of L-Type Calcium channels and decreased Ca2+ levels, which results in vasodilation. Activation of PKG leads to inhibition of IP3R, Ca2+ export and activation of MLC phosphatase, resulting in smooth muscle relaxation. cGMP activates PDE1, 2 and 4 but inhibits PDE3 to regulate degradation of cAMP. Binding of cGMP to PDE5 is vital for regulation of cGMP levels and ultimately controls vasodilation and penile erection.Aging along with vascular, hormonal or neurological irregularities alter production of NO and disturb the balance between synthesis and degradation of cGMP causing ED. The most common anti-impotence drug Sildenafil, which is marketed under the trade name Viagra, acts as a relatively specific vasodilator of the penile circulation that enhances prolonged muscle relaxation/vasodilation by inhibiting the action of PDE5 to increase cGMP levels.

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