The purpose of this study was to examine the role of angiotensin II (ANG II), arginine vasopressin (AVP), and neurogenic mechanisms in maintaining arterial pressure (MAP) in conscious water-deprived rabbits. Water deprivation produced marked increases in plasma renin activity and the concentration of AVP; however, plasma catecholamine concentrations were unchanged. Arterial baroreflex control of renal sympathetic nerve activity (RSNA) and heart rate (HR) was similar in water-replete and dehydrated animals. Administration of an ANG II receptor antagonist (ANG IIX) to water-deprived animals produced a small decrease in MAP but no significant changes in HR or mesenteric and hindquarters vascular resistances. Similarly, there was no significant effect on MAP, HR, or regional hemodynamics when dehydrated animals received an AVP-V1 antagonist (AVPX). RSNA increased by maximums of 61 and 43% in response to ANG IIX and AVPX, respectively. Combined administration of ANG IIX and AVPX produced significant decreases in MAP (-9 mmHg) and hindquarters resistance (-24%) and 117% and 23 beat/min inceases in RSNA and HR, respectively. The effect on mesenteric resistance was variable; however, the response was generally a decrease. We conclude that ANG II and AVP pressor mechanisms are activated to sustain MAP in the dehydrated state. In contrast, the basal level and baroreflex control of sympathetic nervous system activity are unchanged from the water-replete state. However, activation of sympathetic nerve activity may become important in maintaining peripheral resistance when ANG II and AVP receptors are blocked in water-deprived animals.
|Original language||English (US)|
|Journal||American Journal of Physiology - Regulatory Integrative and Comparative Physiology|
|State||Published - 1988|
ASJC Scopus subject areas
- Physiology (medical)