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Losartan attenuates cardiac remodeling but does not prevent vascular dysfunction in isoproterenol‐treated rats
Author(s) -
Davel Ana Paula,
Victorio Jamaira Aparecida,
Clerici Stefano Piatto,
Rossoni Luciana Venturini
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1093.7
Subject(s) - losartan , phenylephrine , contractility , sodium nitroprusside , medicine , endocrinology , angiotensin ii , nitric oxide synthase , contraction (grammar) , aorta , nitric oxide , agonist , chemistry , receptor , blood pressure
Overactivation of β‐adrenoceptors (β‐AR) induced by isoproterenol (Iso) results in cardiac remodeling and vascular dysfunction. We tested the hypothesis that angiotensin II (AII) via AT 1 receptor could be involved in the cardiovascular effects of Iso treatment. Rats were treated with Iso (0.3 mg/kg/day, s.c. ) or vehicle and co‐treated or not with the AT 1 receptor antagonist losartan (Los, 40 mg/kg/day, p.o. ) for one week. Mean arterial pressure and heart rate were not changed by treatments. Iso enhanced right and left ventricular mass and Los attenuated this effect. In aortas, the relaxation responses to acetylcholine and sodium nitroprusside were similar among groups. Iso increased the contractile response of aorta to phenylephrine (Phe) and Los did not alter this effect. Incubation with the inhibitor of nitric oxide (NO) synthase L‐NAME abolished differences in Phe contraction among groups. Data suggest that blockade of AT 1 receptor with Los partially prevents the cardiac remodeling induced by Iso, but not the enhanced contractility of aorta related to a reduced NO modulation. Thus, AII via AT 1 receptor seems do not mediate the vascular effects of β‐AR overactivity. Financial support: FAPESP/Brazil