Vasoconstriction during volume expansion is independent of central control

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 autoregulation 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 vasoconstriction 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).