Decreased influence of nitric oxide on deoxycorticosterone acetate (DOCA)-salt hypertension.

The response to exogenous administration of acetylcholine and the effects of nitric oxide (NO) synthesis blockade were assessed for small arterioles in the cremaster muscle of deoxycorticosterone acetate (DOCA)-salt hypertensive and normotensive rats using intravital microscopy. The NO synthesis inhibitor N omega-L-nitro-arginine methyl ester (L-NAME) produced significantly less constriction in the arterioles of DOCA-salt hypertensive rats. Exposure to increasing concentrations of acetylcholine (10(-10) to 10(-5) mol/L) or sodium nitroprusside (10(-10) to 10(-5) mol/L) produced similar arteriolar dilation in both groups. These results suggest that attenuated basal release of NO by arterioles may play a role in the development of increased peripheral resistance observed in DOCA-salt hypertension.