title: [Duality of angiotensin II receptors and risk for stroke and cancer: what is the connection?].
abstract: Angiotensin II (AII) acts by 2 types of receptors: the ATI receptor which mediates its actions on vasoconstriction, renin (inhibition) and aldosterone (stimulation) secretions, cellular proliferation and angiogenesis and the non-AT1 (often called AT2) receptors. Mainly expressed in the embryon these latter may favor cellular differentiation and recruitment of collateral circulation. Angiotensin converting enzyme inhibitors (ACEI) decrease the synthesis of All and therefore the stimulation of both receptor types whereas AT1-receptor antagonists (AT1RA) block only the stimulation of these latter and increase the stimulation of AT2 receptor since they increase the production of All secondarily to the inhibition of the feedback of renin secretion by All. Experimentally ACEI and AT1RA decrease angiogenesis and cellular proliferation and favor cellular differentiation which could explain the protective effect of ACEI against cancer suggested recently in a Scotish study. Despite of their common suppressive effect on angiogenesis AT1RA may better than ACEI protect against ischemic events specially the cerebral ones because they favor the rapid recruitment of collateral circulation. This has been demonstrated for losartan in case of abrupt ligation of the carotid in the gerbil since its previous administration protects against fatal cerebral ischemia whereas its previous administration with enalapril abolishes this protection. These data may explain why, in the CAPP trial, captopril which has prevented more effectively diabetes occurrence could not be proved superior to diuretics and/or betablocker in the prevention of myocardial infarction and specially of strokes for which exist on the contrary a suspicion of a lower protection. Therefore a comparative trial between AT1RA and ACEI in the prevention of stroke recurrence should appear as a priority for Public Health and Pharmaceutical Industry Authorities.
authors.forename: A
authors.initials: A
authors.lastname: Fournier
authors.forename: A
authors.initials: A
authors.lastname: Ghitu
authors.forename: R
authors.initials: R
authors.lastname: Darabont
authors.forename: H
authors.initials: H
authors.lastname: Mazouz
authors.forename: R
authors.initials: R
authors.lastname: Makdassi
authors.forename: S
authors.initials: S
authors.lastname: Canaple
authors.forename: A
authors.initials: A
authors.lastname: Rosa
authors.forename: L A
authors.initials: LA
authors.lastname: Fernandez
mesh_terms: D000804:Angiotensin II / Q000009:adverse effects*; D002561:Cerebrovascular Disorders / Q000139:chemically induced*; D006801:Humans; D009369:Neoplasms / Q000139:chemically induced*; D011945:Receptors, Angiotensin / Q000187:drug effects; D012307:Risk Factors
chemical_list: D011945:Receptors, Angiotensin; D000804:Angiotensin II