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Captopril (SQ 14225) depresses drinking and aldosterone in rats lacking vasopressin


Angiotensin II is dipsogenic, and vasopressin (ADH) regulates renal water excretion. Together, these hormones govern overall mammalian water balance1,2. The Brattleboro rat with inherited diabetes insipidus (DI) lacks ADH and is therefore a convenient model with which to elucidate mechanisms regulating water metabolism. In the present studies, angiotensin II has also been removed from DI rats by the administration of an inhibitor (captopril, SQ 14225; D-2-methyl-3-mercaptopropanoyl-L-proline) of the enzyme which converts angiotensin I, the relatively inert component of the renin–angiotensin system, to angiotensin II, the biologically active substance3. SQ 14225 reduced the drinking rates, and after 6 days lowered peripheral plasma aldosterone concentrations were associated with hyperkalaemia. We conclude that the polydipsia of diabetes insipidus partly results from elevated plasma renin activities and angiotensin II concentrations seen in this syndrome. Further, the apparent hypoaldosteronism of DI Brattleboro rats reflects differences in both tissue usage of the steroid and adrenocortical sensitivities associated with polyuria, hyperosmolarity and possibly potassium wasting4,5.

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Henderson, I., McKeever, A. & Kenyon, C. Captopril (SQ 14225) depresses drinking and aldosterone in rats lacking vasopressin. Nature 281, 569–570 (1979).

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