Central administration of porcine relaxin stimulates drinking behaviour in rats: an effect mediated by central angiotensin II.

Central injection of porcine relaxin into the lateral ventricle of water-replete rats caused a marked drinking response. Relaxin in 2 µL 0.9% saline caused a dose-dependent (range 10-50 ng), significant (P<0.01) dipsogenesis compared with saline-treated controls. There was no drinking response to <10 ng relaxin. At 10 ng relaxin ICV rats drank 4.2 ± 0.2 mL water within 15 min of injection. The amount of water taken increased with increasing dose and plateaued at 50 ng ICV (10.2 ± 1.3 mL) thereafter; increasing the dose of relaxin did not significantly increase the total volume of water consumed. In contrast, there was no significant increase in water consumed in rats treated with a deactivated form of porcine relaxin, or with insulin. Rats appeared to compensate for the period of hyperdipsia, as there was no significant difference in the water consumed in control (saline-injected) and relaxin-treated rats in the 23 h period after testing.The effect of blocking the central action of angiotensin II on the dipsogenic effects of relaxin was tested by infusing of a specific angiotensin II receptor antagonist into the lateral ventricle before treatment with relaxin. Antagonism of the central angiotensin II system, confirmed by lack of a dipsogenic response to ICV exogenous angiotensin II (10 ng), completely blocked the dipsogenic response of relaxin (50 ng in 1 µL) in female rats.These data demonstrate that exogenous porcine relaxin is dipsogenic in the rat and that the mechanism of action appears to be through the central angiotensin II system. It is possible that relaxin may affect water intake during pregnancy when relaxin levels are detectable in the plasma and the hormone may be implicated in the regulation of cardiovascular function in pregnancy.