Nitric oxide-mediated vasodilatory effect of atrial natriuretic peptide in forearm vessels of healthy humans.

1. The aim of the present study was to determine whether the vasorelaxant effect of atrial natriuretic peptide (ANP) is, in part, endothelium dependent in humans. 2. We used veno-occlusive plethysmography to measure forearm blood flow (FBF) during intra-arterial infusions of ANP (4, 8, 16, 32 pmol/min per dL forearm tissue volume) before and after the inhibition of nitric oxide (NO) synthesis by N(G)-monomethyl-L-arginine (L-NMMA; 100 micromol) in seven normal healthy subjects. 3. Atrial natriuretic peptide caused a dose-dependent increase in FBF both before and after L-NMMA and significantly reduced the plasma concentration of angiotensin (Ang) II. Administration of L-NMMA significantly diminished the increase in FBF in response to ANP infusion (P < 0.05). 4. These results suggest that the forearm vasodilative response to ANP is modulated, in part, by an endothelium-derived NO-mediated mechanism associated with a decrease in AngII caused by ANP.