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Angiotensin II type 1 receptor antagonist versus angiotensin I‐converting enzyme inhibitor in experimental renal diseases
Author(s) -
Jover Bernard,
Demeilliers Bénédicte
Publication year - 2000
Publication title -
fundamental and clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.655
H-Index - 73
eISSN - 1472-8206
pISSN - 0767-3981
DOI - 10.1111/j.1472-8206.2000.tb00438.x
Subject(s) - angiotensin ii receptor type 1 , angiotensin ii , angiotensin converting enzyme , angiotensin receptor , endocrinology , medicine , ace inhibitor , pharmacology , renin–angiotensin system , kidney , endothelin receptor , chemistry , receptor antagonist , receptor , antagonist , blood pressure
— Angiotensin II has an important role in the structural and functional regulation of the cardiovascular and renal systems. Blockade of the renin‐angiotensin system can be achieved with angiotensin‐converting enzyme (ACE) inhibitors and non‐peptidic, orally active, angiotensin II type 1 receptor (ATI) antagonists. However, the question that has yet to be answered is whether ACE inhibitors and ATI receptor antagonists have similar renoprotective effects in various experimental diseases. Although many studies have assessed the role of either ACE inhibitors or ATI receptor antagonists, we have reviewed the literature comparing both types of blocker in the same experiment. In most models of hypertension or renal failure, both classes of blocker appear to have similar antihypertensive and renal profiles. In a few models, the influence of the ACE inhibitor on arterial pressure and/or renal function is more marked than that of the ATI receptor antagonist. Even though the maximum dose‐effect curve for each compound was not often carried out for the systemic haemodynamics and renal alterations, the difference between both classes of blocker, when observed, appeared to favour the participation of non‐angiotensin II or non‐ATI‐mediated mechanisms. Among them are the stimulation of prostaglandin production, kinin accumulation, nitric oxide generation and modulation of endothelin or TGFβ1 expression via direct or indirect pathways. Future experimental and probably human studies aimed at comparing angiotensin II receptor antagonists and ACE inhibitors, with respect to blood pressure and renal damage, should be designed with all these concerns in mind.