Role of nitric oxide in modulating systemic pressor responses to different vasoconstrictors in man.

摘要: OBJECTIVE Animal studies suggest that nitric oxide (NO) attenuates responses to endogenous vasoconstrictors. We investigated whether this also holds true in man by monitoring pressor different vasoconstrictors during synthase (NOS) inhibition. METHODS Systemic hemodynamic intravenous infusions of three doses (each for 5 min) angiotensin II (AngII) (2, 4 and 8 ng/kg per min), noradrenaline (NOR) (10, 30 70 phenylephrine (PE) (0.5, 1.0 1.5 microg/kg were monitored 44 healthy subjects saline. A second dose-response curve was obtained NOS inhibition with a subpressor dose N- nitro-L-arginine-methyl ester (L-NAME) (5 or systemic NO clamp using combined L-NAME (12.5 nitroprusside. Blood pressure measured the brachial artery other parameters derived from signal. RESULTS Mean arterial (MAP) increased 2 +/- 2, 6 1 16 mmHg response AngII saline, 7 6, 15 26 (P < 0.05) 11 10, 18 25 0.001). These augmented MAP due enhanced increments vascular resistance. Infusions NOR PE saline resulted dose-dependent comparable magnitude as those seen AngII, but not affected CONCLUSION Our findings show evoked PE, is inhibition, suggesting associated release counteracts its blood rising effect.