Ramirez-Gil J F, Delcayre C, Robert V, Wassef M, Trouve P, Mougenot N, Charlemagne D, Lechat P
Laboratoire de Pharmacologie Cardiovasculaire, Institut Federatif de Recherche de Génetique et Physiopathologie Cardiovasculaire INSERM-Hôpital Pitié-Salpêtrière, Hôpital Pitié-Salpêtrière, Paris, France.
J Cardiovasc Pharmacol. 1998 Dec;32(6):927-34. doi: 10.1097/00005344-199812000-00009.
Cardiac fibrosis is linked to aldosterone-induced hypertension, but the effects on in vivo left ventricular (LV) function are not established. We studied the relations between in vivo LV function and aldosterone/salt cardiac fibrosis. Adult guinea pigs (GPs) were treated for 3 months with an aldosterone infusion and high-salt diet. This treatment induced arterial hypertension (+35%) and moderate LV hypertrophy (LVH; +60%) without right ventricular (RV) hypertrophy. Echo-Doppler LV assessment demonstrated unaltered cardiac output, stroke volume, or LV relaxation. Type I collagen messenger RNA (mRNA) was significantly increased in both ventricles (LV, +48%; RV, +77%) and accompanied by a significant increase in total collagen deposition (LV, from 0.52% in controls to 4.4% in treated GPs; RV, from 0.82 to 5.5% in treated GPs). Plasma norepinephrine levels increased 2.6-fold (p < 0.01) and correlated with the increase in collagen deposition in both ventricles. Collagen content was not correlated with hypertension or LVH. We conclude that aldosterone administration induces cardiac collagen accumulation and a sympathetic stimulation, which might preserve systolic and diastolic function.