Functional significance of contractile proteins in cardiac hypertrophy and failure.
The functional significance of alterations in contractile proteins was investigated in the chronically overloaded left ventricle of Goldblatt rats and spontaneously hypertensive rats (SHRs). Congestive cardiac insufficiency occurring in late stages of pressure overload is associated with impaired contractility, as well as significant structural dilatation. Only in the event of extreme dilatation, however, would pumping failure occur in the presence of intact myocardial contractile capability. The transformation toward a slower myocardium is associated with a reduced rate of Ca2+ uptake by the sarcoplasmic reticulum. Transformation influences ventricular and myocardial working capacity to a much lesser extent than do the velocity parameters of contraction. Although a fairly homogeneous VM-3 pattern is typical for ventricles when cardiac failure is experimentally induced, extreme myocardial transformation, as such, does not cause congestive failure. With cardiac insufficiency, left ventricular volume, systolic wall stress, and hydroxyproline concentration are overproportionately increased, as related to VM-3 content, whereas noradrenaline content is decreased. This is consistent with the assumption that myocardial transformation is not necessary for the development of these alterations. Myocardial transformation may be promoted by structural dilatation. Extreme transformation, however, should, in turn, decrease contractility, contributing to cardiac failure. A considerable decrease in contractility indirectly causes depletion of the catecholamine stores. The energy-saving effect of myocardial transformation toward a slower muscle cannot compensate for the unfavorable effects of a substantial degree of ventricular dilatation.
Jacob
R
R
Physiologisches Institut II, Universität Tübingen, F.R.G.
Kissling
G
G
Rupp
H
H
Vogt
M
M
D000818:Animals; D006332:Cardiomegaly / Q000503:physiopathology*; D003285:Contractile Proteins / Q000502:physiology*; D006333:Heart Failure / Q000503:physiopathology*; D006973:Hypertension / Q000503:physiopathology; D006977:Hypertension, Renal / Q000503:physiopathology; D051381:Rats; D011918:Rats, Inbred SHR
D003285:Contractile Proteins