The cardiovascular effects of oxytocin in conscious male rats

In conscious, chronically instrumented normotensive male Wistar rats intravenous (i.v.) administration of oxytocin (OXT) (⩾ 100 ng) induced a dose-related biphasic change in mean arterial pressure (MAP). This consisted of an initial pressor effect accompanied by bradycardia and a decrease in cardiac output (CO), followed by a more prolonged fall in MAP which reached a maximum 30 min after injection and was accompanied by an increase in CO. The more specific (Thr4, Gly7]OXT analogue (0.01–10 μg i.v.) caused a dose-related fall in MAP and a rise in CO which reached a maximum after 15–30 min. Similarly in spontaneously hypertensive rats of the stroke prone strain (SHRSP) an initial pressor effect and delayed fall in MAP were apparent after OXT (0.1 and 10 μg i.v.) only the decrease in MAP being evident with the [Thr4, Gly7]OXT analogue. These responses were significantly larger than those observed in Wistar Kyoto controls. The pressor effects are therefore interpreted to be due to vasopressin receptor activation while the depressor effects appear to be oxytocin specific. In sinoaortic denervated rats, OXT (0.1 and 10 μg i.v.) induced an enhanced initial pressor effect with a much reduced reflex bradycardia and fall in CO. A larger and more prolonged delayed fall in MAP was apparent with both OXT and [Thr4, Gly7]OXT accompanied by a decrease in CO when compared to sham-operated controls. Intracisternally (i.c.) administered OXT (0.05–10 ng) had no effect on MAP or heart rate. However OXT and [Thr4, Gly7]OXT (10 ng i.c.) caused a decrease in baroreflex sensitivity in response to both a rise and a fall in MAP induced by phenylephrine (1 μg) and sodium nitroprusside (13 μg) respectively. It is concluded that OXT is involved in cardiovascular regulation, inducing a decrease in baroreflex sensitivity upon central administration and a fall in MAP when injected i.v.