Angiotensin II-nitric oxide interaction on sympathetic outflow in conscious rabbits

Circulation Research
J L LiuI H Zucker

Abstract

Increasing evidence suggests that endogenous NO inhibits sympathetic outflow in anesthetized animals. However, in a recent study from this laboratory, we were unable to find any evidence of increased renal sympathetic nerve activity (RSNA) in response to blockade of NO synthesis in conscious rabbits. Because angiotensin II (Ang II) increases sympathetic outflow, one factor for this discrepancy may be the difference in the resting level of Ang II, which may be lower in well-trained conscious animals. In the present study, the effects of blockade of NO synthesis with Nomega-nitro-L-arginine methyl ester (L-NAME, 30 mg/kg IV) on resting RSNA with and without a background intravenous infusion of Ang II (10 ng.kg(-1).min(-1)) was investigated in conscious rabbits. Intravenous administration of L-NAME (30 mg/kg) caused an increase in mean arterial blood pressure (MAP, from 80.4+/-2.9 to 92.8+/-2.5; P=.0001) and a decrease in RSNA (from 100+/-0% to 53.4+/-8.6%, P=.0016). When the elevated blood pressure was returned to control by infusion of hydralazine (0.01 to 0.06 mg.kg(-1).min(-1)), RSNA returned to the level before L-NAME administration. During a sustained infusion of Ang II (10 ng.kg(-1).min(-1)), L-NAME increased MAP from 89.2+...Continue Reading

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Jul 17, 1999·The American Journal of Physiology·J L LiuI H Zucker
May 17, 2001·American Journal of Physiology. Regulatory, Integrative and Comparative Physiology·J L LiuI H Zucker

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