Key result
Inhibition of nitric oxide synthesis with L-NMMA significantly diminished the dose-dependent increase in forearm blood flow caused by atrial natriuretic peptide infusion (P<0.05).
Why the study?
Does nitric oxide synthesis inhibition diminish the vasodilatory effect of atrial natriuretic peptide in forearm vessels of healthy humans?
Does nitric oxide synthesis inhibition diminish the vasodilatory effect of atrial natriuretic peptide in forearm vessels of healthy humans?
p-value: p=<0.05
The vasodilatory effect of atrial natriuretic peptide in human forearm vessels is partially mediated by endothelium-derived nitric oxide, associated with a decrease in angiotensin II.
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.
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Sugamori et al. (2002) studied Healthy (n=7). Atrial natriuretic peptide (ANP) infusion with and without L-NMMA vs. ANP infusion before L-NMMA was evaluated on Forearm blood flow (FBF) (p=<0.05). Inhibition of nitric oxide synthesis with L-NMMA significantly diminished the dose-dependent increase in forearm blood flow caused by atrial natriuretic peptide infusion (P<0.05).
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