Summerlee A J, Robertson G F
Department of Biomedical Sciences, Ontario Veterinary College, University of Guelph, N1C 2W1, Ontario, Canada.
Endocrine. 1995 May;3(5):377-81. doi: 10.1007/BF03021422.
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.
向水合充足的大鼠侧脑室内中央注射猪松弛素会引发明显的饮水反应。与用生理盐水处理的对照组相比，2微升0.9%生理盐水中的松弛素引起了剂量依赖性（范围为10 - 50纳克）的显著（P<0.01）饮水增多。对低于10纳克的松弛素没有饮水反应。注射10纳克松弛素后，脑室内注射的大鼠在15分钟内饮用了4.2±0.2毫升水。饮水量随剂量增加而增加，在脑室内注射50纳克后达到平稳状态（10.2±1.3毫升）；增加松弛素剂量并未显著增加总饮水量。相比之下，用失活形式的猪松弛素或胰岛素处理的大鼠饮水量没有显著增加。大鼠似乎对多饮期进行了代偿，因为在测试后的23小时内，对照组（注射生理盐水）和松弛素处理组大鼠的饮水量没有显著差异。在用松弛素处理前，通过向侧脑室内注入特异性血管紧张素II受体拮抗剂来测试阻断血管紧张素II的中枢作用对松弛素饮水作用的影响。对脑室内注射外源性血管紧张素II（10纳克）无饮水反应证实了中枢血管紧张素II系统的拮抗作用，这完全阻断了雌性大鼠对松弛素（1微升中50纳克）的饮水反应。这些数据表明，外源性猪松弛素在大鼠中具有致渴作用，其作用机制似乎是通过中枢血管紧张素II系统。在孕期血浆中可检测到松弛素水平时，松弛素可能会影响水摄入，并且该激素可能参与孕期心血管功能的调节。
