title: Role of central AT1 and V1 receptors in cardiovascular adaptation to hemorrhage in SD and renin TGR rats.
abstract: 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.
authors.affiliation: Department of Experimental and Clinical Physiology, Medical University of Warsaw, 00-927 Warsaw, Poland.
authors.forename: P
authors.initials: P
authors.lastname: Paczwa
authors.forename: E
authors.initials: E
authors.lastname: Szczepańska-Sadowska
authors.forename: S
authors.initials: S
authors.lastname: Loń
authors.forename: S L
authors.initials: SL
authors.lastname: Ganten
authors.forename: D
authors.initials: D
authors.lastname: Ganten
mesh_terms: D000222:Adaptation, Physiological / Q000502:physiology*; D057911:Angiotensin Receptor Antagonists; D000818:Animals; D030801:Animals, Genetically Modified / Q000235:genetics; D065092:Antidiuretic Hormone Receptor Antagonists; D001921:Brain / Q000378:metabolism*; D002319:Cardiovascular System / Q000503:physiopathology*; D006470:Hemorrhage / Q000503:physiopathology*; D006973:Hypertension / Q000235:genetics / Q000503:physiopathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D044140:Receptor, Angiotensin, Type 1; D044139:Receptor, Angiotensin, Type 2; D011945:Receptors, Angiotensin / Q000378:metabolism*; D017483:Receptors, Vasopressin / Q000378:metabolism*; D012016:Reference Values; D012083:Renin / Q000235:genetics / Q000378:metabolism*
chemical_list: D057911:Angiotensin Receptor Antagonists; D065092:Antidiuretic Hormone Receptor Antagonists; D044140:Receptor, Angiotensin, Type 1; D044139:Receptor, Angiotensin, Type 2; D011945:Receptors, Angiotensin; D017483:Receptors, Vasopressin; D012083:Renin