Experiments were conducted to investigate the role of the brain angiotensin system in mediating the pressor effects of porcine relaxin in anesthetized female rats. Continuous intracerebroventricular infusion of a specific angiotensin II receptor antagonist (Sar1-Ala8-angiotensin II) completely negated the pressor response to centrally administered relaxin, but only partially suppressed the increase in blood pressure observed after iv injection of the hormone. These results indicate that the pressor effects of relaxin may be mediated, at least in part, by brain angiotensin. Rats with a compromised central angiotensin system were then treated in combination with a peripheral vasopressin (V1) receptor antagonist. Only after both treatments were the pressor effects of iv relaxin completely negated. These data imply that there is also a significant pressor action of relaxin which is independent of the brain angiotensin system. The most likely alternative is a direct action of relaxin on the neural lobe of the pituitary, to provoke the release of vasopressin.