title: Time-dependent changes of left ventricular contractility in Langendorff perfused hearts from renovascular hypertensive rats.
abstract: 1. The contractile activity of the hypertrophied myocardium was investigated in Langendorff perfused hearts from one-kidney one-clip (1K1C) renovascular hypertensive rats. 2. Hearts obtained from control and renovascular hypertensive animals were studied 15, 30 and 60 days after sham operation (SO) or renovascular hypertension induction. Rats were anesthetized with ether and mean blood pressure (MBP) and heart rate (HR) were measured. The hearts were then excised and perfused with Krebs solution and bicarbonate buffer, at 31 degrees C, with a perfusion pressure of 75 mmHg, beating spontaneously. The left ventricular function curves were evaluated by measuring the isovolumic systolic pressure (ISP) obtained at diastolic pressures (DP) of 0, 10, 20 and 30 mmHg in 0.62, 1.25 and 2.5 mM extracellular calcium. After the experiments the left ventricle (LV) was dissected, blotted and dried to obtain the dry and wet weights. 3. The 1K1C animals were hypertensive and displayed LV hypertrophy. The LV function curves showed the expected behavior, being similar for all 3 calcium concentrations used for the 15-day groups. However, at 30 days, ISPs were lower than those from the SO control group. Moreover, after 60 days ISPs from 1K1C rat ventricles were higher than controls in 0.62 mM calcium for all DPs. For all other DPs, ISP from 1K1C and control ventricles were similar. Normalization of ISP to LV dry weight showed that the hypertrophied ventricles, at any time and at all calcium concentrations used, developed less pressure by ventricular mass than SO controls. 4. Absolute ISP results suggest changes in the contractile machinery characteristics, not only as a function of the pressure overload but also as a function of the hypertension time course, and that ISP normalization to ventricular mass demonstrated the lower capacity of the hypertrophied muscle to generate force and pressure.
authors.affiliation: Departamento de Ciências Fisiológicas, Universidade Federal do Espírito Santo, Vitória, Brasil.
authors.forename: R H
authors.initials: RH
authors.lastname: Kioshi
authors.forename: I
authors.initials: I
authors.lastname: Stefanon
authors.forename: J G
authors.initials: JG
authors.lastname: Mill
authors.forename: D V
authors.initials: DV
authors.lastname: Vassallo
mesh_terms: D000818:Animals; D001794:Blood Pressure; D006339:Heart Rate; D006978:Hypertension, Renovascular / Q000503:physiopathology*; D017379:Hypertrophy, Left Ventricular / Q000503:physiopathology*; D007552:Isotonic Solutions / Q000008:administration & dosage; D008297:Male; D009200:Myocardial Contraction / Q000502:physiology*; D010477:Perfusion; D051381:Rats; D013997:Time Factors; D016277:Ventricular Function, Left / Q000502:physiology*
chemical_list: D007552:Isotonic Solutions; C051865:Krebs-Ringer solution