Molecular mechanisms for the regulation of penile smooth muscle contractility.
Relaxation of smooth muscle is viewed as a 'resetting' of contractile machinery and the resumption of a pre-contractile state is accomplished by lowering cytosolic Ca(2+) and/or by decreasing the sensitivity of the contractile machinery to Ca(2+). There are several mechanisms whereby cytosolic Ca(2+) can be reduced and relaxation achieved but, in general, all pathways depend upon the accumulation of cyclic nucleotides cAMP and cGMP or on the activation of K(+) channels resulting in hyperpolarization. Recently, activation of Na(+)/K(+) ATPase by nitric oxide has been shown to be involved in the relaxation of trabecular smooth muscle. Since Na(+)/K(+) ATPase is electrogenic, its stimulation would cause hyperpolarization and, in turn, would prevent the opening of voltage-dependent Ca(2+) channels. This manuscript briefly reviews the molecular mechanisms affected by muscle relaxants and vasodilators in the treatment of erectile dysfunction. International Journal of Impotence Research (2000) 12, Suppl 4, S34-S38.
Saenz de Tejada
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Departmento de Investigacion, Hospital Ramon y Cajal, Madrid, Spain. fundacion@coronadoserv.com
D000242:Cyclic AMP / Q000378:metabolism; D006152:Cyclic GMP / Q000378:metabolism; D004594:Electrophysiology; D006801:Humans; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000166:cytology / Q000502:physiology*; D009569:Nitric Oxide / Q000502:physiology; D010413:Penis / Q000502:physiology*; D014661:Vasoconstriction / Q000502:physiology*
D009569:Nitric Oxide; D000242:Cyclic AMP; D006152:Cyclic GMP