Vasoconstriction, RhoA/Rho-kinase and the erectile response.
Recent studies have suggested that contraction of the smooth muscle in the cavernosal arterioles and in the walls of the cavernosal sinuses is maintained by the RhoA/Rho-kinase signaling pathway. However, this contraction activity must be overcome to permit the vasorelaxation essential for erection. We postulate that nitric oxide (NO) causes erection primarily by inhibiting the RhoA/Rho-kinase pathway. The following will discuss evidence in support of the important role of Rho-kinase-mediated vasoconstriction in the nonerect penis and how NO overrides this Rho-kinase-mediated vasoconstriction to permit vasodilation and erection.
Mills
T M
TM
Department of Physiology, Medical College of Georgia, Augusta, Georgia 30912-3000, USA.tmills@mail.mcg.edu
Lewis
R W
RW
Wingard
C J
CJ
Linder
A E
AE
Jin
L
L
Webb
R C
RC
D006801:Humans; D047908:Intracellular Signaling Peptides and Proteins; D008297:Male; D009130:Muscle, Smooth / Q000502:physiology; D010410:Penile Erection / Q000502:physiology*; D010413:Penis / Q000098:blood supply / Q000201:enzymology; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism*; D014661:Vasoconstriction / Q000502:physiology*; D054460:rho-Associated Kinases; D020742:rhoA GTP-Binding Protein / Q000378:metabolism*
D047908:Intracellular Signaling Peptides and Proteins; D017346:Protein Serine-Threonine Kinases; D054460:rho-Associated Kinases; D020742:rhoA GTP-Binding Protein