Why the study?
Does the oral converting enzyme inhibitor SQ 14225 alter hemodynamics and sodium excretion in dogs with experimental high output failure?
Does the oral converting enzyme inhibitor SQ 14225 alter hemodynamics and sodium excretion in dogs with experimental high output failure?
The converting enzyme inhibitor SQ 14225 reduces arterial pressure and plasma aldosterone while increasing sodium excretion over 3 days, demonstrating the role of the renin-angiotensin-aldosterone system in experimental high output failure.
ACE inhibition lowers pressure and aldosterone in canine high-output failure; leaves open translation to human HF therapy.
The relation of the renin-angiotensin-aldosterone system to sodium retention was studied in dogs with an aortic-caval fistula and high output failure by administering orally the new converting enzyme inhibitor SQ 14225. The acute response to an initial oral dose of SQ 14225 (10 mg/kg) consisted in a fall in arterial pressure (BP) from 97 to 67 mmHg, plasma aldosterone concentration (PAC) from 21.7 to 11.3 ng/100 ml, creatinine clearance (CCr) from 89 to 44 ml/min, and filtration fraction (FF) from 39 to 18%, whereas plasma renin activity (PRA) increases from 12.7 to 36.1 ng angiotensin I.ml-1.h-1 and renal sodium excretion was unchanged. It is suggested that the marked fall in BP and CCr offset the drop in PAC and FF which favored a natriuresis. The daily responses to SQ 14225 for 3 days also showed a fall in BP and PAC but sodium excretion increased. In the animal with the best response, a striking natriuresis occurred. These findings demonstrate an important role for the renin-angiotensin-aldosterone system in experimental high output failure.
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Williams et al. (1979) studied this question.
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