Role of ANG II in hypertension produced by chronic inhibition of nitric oxide synthase in conscious rats

These experiments tested the hypothesis that hypertension caused by chronic inhibition of nitric oxide synthase (NOS) is associated with augmented presser responsiveness to angiotensin II (ANG II). Antagonism of ANG II AT(1) receptors with losartan caused a greater fall in blood pressure (BP) in rats treated for 2 wk with the NOS inhibitor N-omega-nitro-L-arginine methyl ester (L-NAME) than in normotensive rats. The delayed time course of the decline in BP implicated the slow presser effect (SPE) of ANG II in L-NAME hypertension. Further experiments showed that direct elicitation of the SPE by continuous low-dose (4 ng/min) intravenous infusion of ANG II in enalapril-treated rats resulted in a larger chronic increase in BP if NOS was inhibited. However, L-NAME alone also caused a significant increase in BP in enalapril-treated rats. The combined effect on BP of ANG II and L-NAME was merely additive. These results confirm that ANG II is involved in L-NAME hypertension. However, chronic presser responsiveness to the peptide is not augmented by L-NAME.