VASOCONSTRICTION DURING VOLUME EXPANSION IS INDEPENDENT OF CENTRAL CONTROL

被引:7
作者
HINOJOSALABORDE, C
THUNHORST, RL
COWLEY, AW
机构
[1] Department of Physiology, Medical College of Wisconsin, Milwaukee, WI
关键词
Blood pressure; Blood volume; Cardiac output; Central nervous system; Homeostasis; Vasoconstriction;
D O I
10.1161/01.HYP.15.6.712
中图分类号
R6 [外科学];
学科分类号
1002 ; 100210 ;
摘要
We have previously demonstrated that, in the absence of the rapid acting neural and hormonal controllers of blood pressure, an acute blood volume expansion of only 5% in unanesthetized rats caused an increase in total peripheral resistance (TPR) of 22%. Either whole body auto regulation or the release of a putative ouabainlike factor from the central nervous system (CNS) could have explained these responses. The purpose of the present study was to investigate the possible contribution of a centrally released ouabainlike factor to the vasocon-striction response observed during volume expansion. Because the anteroventral third ventricle (AV3V) region is proposed to be important in the control of this putative factor, we compared the hemodynamic responses to blood volume expansion in rats with AV3V lesions (n=6), sham lesions (n=6), and total CNS ablation (n=6). The results of our studies showed that neither AV3V lesion nor CNS ablation reduced the increases of total peripheral resistance seen with blood volume expansion. We conclude that centrally released factors are not required for vasoconstriction in response to acute volume expansion and that regional autoregulatory mechanisms result in a net increase of systemic vascular resistance (i.e., whole body autoregulation). © 1990 American Heart Association, Inc.
引用
收藏
页码:712 / 717
页数:6
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