Why the study?
Does an intravenous peptide converting enzyme inhibitor reduce blood pressure in rabbit models of renal hypertension?
Does an intravenous peptide converting enzyme inhibitor reduce blood pressure in rabbit models of renal hypertension?
This early preclinical study demonstrates that ACE inhibition lowers blood pressure in renin-dependent models of hypertension, establishing its potential utility for investigating and treating clinical hypertension.
Supports ACE inhibition in acute renin-dependent rabbit models; leaves open chronic efficacy and clinical translation.
A peptide converting enzyme inhibitor given intravenously to rabbits was shown to abolish the pressor response to injections of rabbit renin and of angiotensin-I and to augment the depressor response of bradykinin. In rabbits with acute two-kidney Goldblatt hypertension (2-KGH [one renal artery clamped, the other intact]) a total dose of 36 mg/kg infused for one hour lowered the blood pressure but not to a normal level. One week after removal of the intact kidney (acute one-kidney Goldblatt hypertension [1-KGH]) infusions of the peptide were still antihypertensive. Thirty to 60 days after removal of the intact kidney (chronic 1-KGH) the decapeptide had no antihypertensive effects. It is suggested that in the first two models hypertension is dependent on the renin-angiotensin system (RAS), but not in the chronic 1-KGH animal. Since the response to the new agent is not species specific and is well tolerated, it may become a valuable tool in investigating the role of the RAS in various forms of clinical hypertension.
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Romero-Benavides et al. (1974) studied this question.
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