抄録
Nitric oxide plays an important role in the regulation of arterial pressure by its actions to dilate vascular smooth muscle, alter sympathetic neural activity, and modulate the vasoconstrictor action of norepinephrine, angiotensin II and vasopressin. Nitric oxide may also influence blood pressure regulation by altering the secretion of renin and vasopressin. To test this possibility, we investigated the effects of inhibiting nitric oxide synthesis on the cardiovascular, renin and vasopressin responses to hypotensive hemorrhage, a situation in which the renin-angiotensin system and vasopressin contribute significantly to the control of blood pressure. Arterial blood was withdrawn from conscious, chronically-prepared rabbits at 1.0ml/kg/min for 15min under control conditions, and during i.v, infusion of the nitric oxide synthase inhibitor L-NAME. Hemorrhage decreased mean arterial pressure from 69±2 to 45±4mm Hg (p<0.01) and increased heart rate from 211±10 to 270±15bpm (p<0.05). Plasma renin activity increased from 7.7±1 to 36.1±9.6ng/ml/2h at 15min (p<0.01), while plasma vasopressin concentration increased from 1.7±0.6 to 183.2±98.5pg/ml (p<0.05). Infusion of L-NAME increased blood pressure and plasma vasopressin concentration, and decreased heart rate and plasma renin activity. L-NAME markedly attenuated the hypotensive response to hemorrhage (72±3 to 62±4mmHg), but did not alter the increases in heart rate, plasma renin activity or plasma vasopressin concentration. In separate experiments, L-NAME did not alter the setpoint or gain of the baroreceptor reflex control of heart rate. These results demonstrate that inhibition of nitric oxide synthesis significantly improves blood pressure regulation during hemorrhage, but indicate that this improvement is not associated with alterations in the heart rate, renin or vasopressin responses to hemorrhage. (Hypertens Res 1995; 18: 55-61)
