In acute experiments, intracranially applied angiotensin II and vasopressin elicit significant cardiovascular effects. The purpose of the present study was to find out whether chronic intrabrain elevation of these peptides, occurring in the renin transgenic TGR(mRen2)27 (TGR) rats, results in an alteration of the cardiovascular control. Mean arterial blood pressure (MAP) and heart rate responses to hypovolemia were examined in hypertensive TGR and normotensive Sprague-Dawley (SD) rats under control conditions and during blockade of central AT₁ or V₁ receptors. Both groups received cerebroventricular infusions of either 1) cerebrospinal fluid (series 1), 2) AT₁ receptors antagonist (AT₁ANT, series 2), or 3) V₁ receptors antagonist (V₁ANT, series 3). Blockade of AT₁ and V₁ receptors decreased MAP in TGR but not in SD rats. In SD rats, bleeding elicited a similar decrease of MAP in each series and a transient increase of heart rate in series 3. In TGR, hemorrhage caused bradycardia and decrease of MAP, which was greater than in SD rats. Hemorrhagic hypotension in TGR was abolished by V₁ANT and bradycardia by V₁ANT or AT₁ANT. The results demonstrate remarkable differences in cardiovascular adjustment to hemorrhage in SD and TGR rats and provide evidence for enhanced involvement of central V₁ and AT₁ receptors in the regulation of blood pressure during hypovolemia in TGR. Central V₁ vasopressin receptors play a crucial role in eliciting posthemorrhagic hypotension and bradycardia in this strain.

angiotensin; hypertension; losartan; vasopressin; TGR (mRen2)27

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