PRESSOR AND BRADYCARDIAC EFFECTS OF CENTRALLY ADMINISTERED RELAXIN INCONSCIOUS RATS

The current study tested the hypothesis that centrally administered re laxin elevates arterial pressure in conscious rats and that this hyper tensive effect is mediated, at least in part, by central or peripheral vasopressin. Injection of human relaxin (0.068 or 0.34 mu g in 200 nL artificial cerebrospinal fluid) into the right lateral ventricle of c onscious, unrestrained Sprague-Dawley rats caused significant dose-rel ated increases in arterial pressure and decreases in heart rate. The p resser and bradycardic responses to intracerebroventricular injections of relaxin were significantly blunted by pretreatment with either int racerebroventricular or intravenous injection of a vasopressin recepto r (V1) antagonist, suggesting that the cardiovascular effects of centr al relaxin are mediated, at least in part, by V1 receptors in the brai n and perhaps also by vasopressin released into the peripheral circula tion. Neither intracerebroventricular injection of the vehicle alone n or intravenous injection of relaxin (0.34 mu g) altered arterial press ure or heart rate. In contrast to the above, intravenous injections of relaxin (40 mu g/kg) elicited presser and tachycardic responses that were not blunted by pretreatment with either intracerebroventricular o r intravenous injection of the V1 receptor antagonist. Together, these data suggest that in the central nervous system relaxin contributes t o the regulation of cardiovascular function and that the mechanisms fo r the cardiovascular effects of central and peripheral relaxin are dis tinct.