Enhanced nitric oxide synthesis reverses salt-induced alterations in bloodflow and cGMP levels

To understand the role of nitric oxide in salt-induced hypertension, we eva luated cardiovascular, hemodynamic and biochemical parameters in Dahl salt- sensitive rats fed low (0.3%) and high (8.0%) sodium diets. Two high salt g roups received 1.25 and 2.5 g/L 1-arginine in their drinking water. After t hree weeks of treatment, blood pressure was greater in the high salt groups . 1-arginine did not modify salt-induced hypertension. Eicosapentaenoic aci d (EPA) caused a smaller depressor response compared to normotensive rats. The increase in blood pressure was associated with decreases in aortic and renal blood flows. In renal artery, the reduction was counteracted by both 1-arginine doses; whereas in the aorta, only the higher 1-arginine one rest ored blood flow. The salt-induced reduction in aortic cyclic GMP level was only overcome by the higher 1-arginine treatment. These data suggest that a t the dose levels tested, nitric oxide reverses the reduction in cGMP and b lood flow, but not the blood pressure changes associated with salt-induced hypertension.