Involvement of the renin-angiotensin system in the dipsogenic effect of morphine

This paper examined whether drinking elicited by morphine is dependent upon an intact renin-angiotensin system. Bilateral nephrectomy, carried out one day prior to administration of morphine, completely abolished morphine-induced water intake, pointing to involvement of the kidneys in the dipsogenic effect of morphine. Plasma and renal renin depletion were induced by the clipping of one renal artery followed, one month later, by removal of the clipped kidney. In such renin-depleted rats with subnormal plasma renin levels, morphine and isoprenaline-induced water intakes were linearly related to pre-injection basal plasma renin level. Such a relationship was not found in rats with normal renin levels. These results pointed to the existence of a permissive interaction between morphine and the renin-angiotensin system. Captopril, an inhibitor of the angiotensin converting enzyme, increased morphine-induced water intake. We interpreted this drinking response as being the sum of morphine-induced drinking (following a permissive interaction between morphine and circulating angiotensin I or renin) and captopril-induced drinking (following a captopril-induced increase in circulating renin and angiotensin I levels). The competitive antagonist of angiotensin II, saralasin, had no effect on morphine-induced drinking. This result pointed once again to a permissive interaction between morphine and circulating angiotensin I or renin.