Peripheral ACE inhibition paradoxically enhances drinking in rats, while central administration blocks it, highlighting complex renin-angiotensin system mechanisms in thirst.
Peripheral ACE inhibition may enhance thirst in rats; leaves open differential central-peripheral RAS roles for future mechanistic studies.
A competitive angiotensin converting enzyme antagonist SQ 20, 881 (SQ), was used to examine the role of the renin-angiotensin system in putative renin-dependent thirst in the albino rat. Significant enhancement of "renin-dependent" as well as renin-independent drinking was observed in the presence of peripheral SQ. Intraventricular SQ obviated this enhancement of drinking but did not affect the water intake caused by the original stimulus itself, whereas it sharply reduced drinking evoked by peripheral renin in nephrectomized rats. Prior renin depletion likewise had no influence on so-called renin-dependent thirst.
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Lehr et al. (1973) studied this question.
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