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Water Drinking in Rats Resulting from Intravenous Relaxin and Its Modification by Other Dipsogenic Factors¹

Howard Florey Institute of Experimental Physiology and Medicine, University of Melbourne, Parkville, Victoria 3052, Australia

Address all correspondence and requests for reprints to: Dr. M. J. McKinley, Howard Florey Institute, University of Melbourne, Parkville, Victoria, 3052 Australia. E-mail: mmck{at}hfi.unimelb.edu.au

The purpose of the study was to determine whether iv infusion of relaxin would acutely stimulate water drinking in rats and, if it did, whether such drinking is affected by other dipsogenic stimuli or is blocked by centrally administered losartan. iv infusions of human gene 2 relaxin at doses of 25, 40, 55, or 80 µg/kg·h for 1 h induced dose-dependent water drinking in both male and female rats within 15–30 min of commencement of infusions. iv infusion of a nondipsogenic dose of angiotensin II (0.5 µg/h), combined with relaxin (40 µg/kg·h), almost tripled the relaxin-induced water intake. iv infusion of hypertonic (1 M) NaCl did not potentiate relaxin-induced drinking. Intracerebroventricular injection of the angiotensin AT₁ antagonist losartan (10 µg) reduced water drinking induced by iv infusion of relaxin.

The water drinking induced by iv infusion of relaxin in the rat suggests that blood-borne relaxin may be a dipsogenic hormone. Potentiation of this relaxin-induced drinking by moderate levels of circulating angiotensin II is additional evidence in support of this view. The results also indicate that a central angiotensinergic neural pathway, utilizing AT₁ receptors, subserves relaxin-induced drinking.

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