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Department of Physiology-7756, The University of Texas Health Science Center at San Antonio, San Antonio, Texas 78229-3900
Acutely increasing
peripheral angiotensin II (ANG II) reduces the maximum renal
sympathetic nerve activity (RSNA) observed at low mean arterial blood
pressures (MAPs). We postulated that this observation could be
explained by the action of ANG II to acutely increase arterial blood
pressure or increase circulating arginine vasopressin (AVP). Sustained
increases in MAP and increases in circulating AVP have previously been
shown to attenuate maximum RSNA at low MAP. In conscious rabbits
pretreated with an AVP V1 receptor antagonist, we compared the effect
of a 5-min intravenous infusion of ANG II (10 and 20 ng · kg
1 · min1) on the
relationship between MAP and RSNA when the acute pressor action of ANG
II was left unopposed with that when the acute pressor action of ANG II
was opposed by a simultaneous infusion of sodium nitroprusside (SNP).
Intravenous infusion of ANG II resulted in a dose-related attenuation
of the maximum RSNA observed at low MAP. When the acute pressor action
of ANG II was prevented by SNP, maximum RSNA at low MAP was attenuated,
similar to that observed when ANG II acutely increased MAP. In
contrast, intravertebral infusion of ANG II attenuated maximum RSNA at
low MAP significantly more than when administered intravenously. The
results of this study suggest that ANG II may act within the central
nervous system to acutely attenuate the maximum RSNA observed at low MAP.
circulating hormones; renal nerves; sympathetic nervous system; blood pressure; kidney
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