Why the study?
Does ACE inhibition with MK 421, SA 446 or captopril reduce blood pressure and alter renal prostaglandin E and kinins in conscious normotensive rats?
Does ACE inhibition with MK 421, SA 446 or captopril reduce blood pressure and alter renal prostaglandin E and kinins in conscious normotensive rats?
The greater hypotensive effect of ACE inhibitors in sodium-depleted rats may be partly due to a stimulated renal kinin system rather than the renal prostaglandin E system.
May implicate renal kinins in ACE inhibitor potentiation during sodium depletion in rats; leaves open human translation.
Angiotensin converting enzyme inhibition by MK 421, SA 446 or captopril (6 mg/kg/day ip) for up to 6 days induced significant fall in systolic blood pressure and plasma angiotensin II concentration. The hypotensive effect was greater in sodium depleted rats than in sodium repleted rats. The hypotensive effect was also accompanied by increased excretion of urinary prostaglandin E2, however the levels of urinary prostaglandin E2 in sodium repleted rats were not different from those in sodium depleted rats. Urinary kinin excretion was increased during infusion of MK 421, SA 446 or captopril in sodium depleted rats, whereas no significant change was found in sodium repleted rats. Thus the present results suggest that renal prostaglandin E system may not be essential for the hypotensive effect of these inhibitors. In addition, the greater hypotensive effect of these inhibitors in sodium depleted rats may be in part due to stimulated renal kinin system.
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Yasujima et al. (1987) studied this question.
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