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Valsartan and coronary haemodynamics in early post‐myocardial infarction in rats
Author(s) -
Gervais Marianne,
Richer Christine,
Fornes Paul,
Gasparo Marc,
Giudicelli JeanFrançois
Publication year - 1999
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.1472-8206.1999.tb00374.x
Subject(s) - valsartan , cardiology , medicine , angiotensin ii , myocardial infarction , hemodynamics , coronary vasodilator , left ventricular hypertrophy , heart failure , vascular resistance , vasodilation , angiotensin ii receptor type 1 , muscle hypertrophy , ventricular remodeling , blood pressure , cardiac fibrosis , ventricular hypertrophy
— Angiotensin 11 AT 1 receptor blockade (AT 1 ) has been shown to prolong survival in post‐myocardial infarction (MI) heart failure in rats. In this study, we investigated whether an early AT ‐ 1 ‐induced improvement in coronary vasodilatation reserve (CVR) might be involved in this beneficial effect. Wistar rats with MI were treated daily and orally for 6 weeks with valsartan, 5 (MI‐V5) or 50 mg/kg (MI‐V50). MI‐controls and sham‐operated rats (S‐controls) received no treatment. Subsequently, systemic and coronary haemodynamics (at baseline and at maximal vasodilatation, CVR fluospheres) were investigated in the conscious state, and cardiac remodelling (hypertrophy and fibrosis) was assessed. As compared to MI‐controls, valsartan (5 mg/kg), had no effect on systemic haemodynamics or myocardial hypertrophy and fibrosis development, gave slightly improved basal left and right ventricular coronary flow and resistance values, but decreased left and right CVR values. Valsartan (50 mg/kg), decreased blood pressure (‐ 11%) and left ventricular end diastolic pressure (‐ 32%), limited the development of cardiac hypertrophy (‐ 19%) but not that of fibrosis, slightly improved basal left ventricular flow and resistance values but only the right ventricular CVR value was increased. We conclude that in rats with post‐MI, an early AT 1 ‐induced improvement in coronary haemodynamics is not responsible for the long‐term survival prolongation observed. Furthermore, that cardiac hypertrophy was prevented whereas fibrosis was not, suggests that the latter is a pivotal determinant of CVR.