Numerous etiological studies have established a positive clinical association between
hypertension and
erectile dysfunction. However, to date, the mechanism underlying this dysfunction remains to be established. In this study, we demonstrate the presence of
erectile dysfunction in two rat models of
hypertension, and hypothesize that increased
vasoconstrictor signaling via
Rho-kinase contributes to the decreased erectile response. We found
deoxycorticosterone-
salt and
stroke prone-spontaneously hypertensive rats to exhibit a decreased erectile response, recorded as intracavernosal pressure/mean arterial pressure (ICP/MAP) upon electrical stimulation of the major pelvic
ganglion. As previously shown, inhibition of
Rho-kinase activity by intracavernosal injection of the selective inhibitor,
Y-27632, resulted in an increase in ICP/MAP. However,
Y-27632 was significantly less effective at increasing ICP/MAP in the hypertensive as compared to normotensive rats. Additionally, intracavernosal injection of
Y-27632 potentiated the voltage-stimulated increase in ICP/MAP in both hypertensive and normotensive rats, but was less effective at potentiating the voltage-mediated erectile response in the hypertensive rats. Altogether, our data demonstrate a decreased erectile response in a
mineralocorticoid and genetic model of
hypertension, and suggest the role of increased cell signaling by
Rho-kinase in the
vasoconstrictor activity of
erectile dysfunction associated with
hypertension.