Cardiac function in experimental hypertension

Abstract

Cardiac growth is controlled by two sets of factors. The first set includes factors that are time dependent and not related to functional demands, which occur mainly in the embryogenic period. The second set is related to the contractile activity of the heart, which depends on the hemodynamic load.’ Despite the different underlying pathophysiologies, pressure or volume overload of the ventricles increases left ventricular systolic or diastolic circumferential wall stress. As defined by the Laplace equation, this is a function of the product of intracavitary pressure (P) times the chamber radius (R) divided by myocardial wall thickness (h): Stress = P . R/2h. In response to the increased stress caused by pressure overload, a rapid biochemical response of the myocardium with increased protein synthesis is induced.2 The intimate mechanism of the induced activation of protein synthesis is presently unresolved. Many factors responsible for the development and maintenance of hypertension may play a role in the stimulation of left ventricular hypertropb. It is known that in hypertensive patients, as well as in different models of experimental hypertension, the extent of cardiac enlargement is not always proportionate to the level of arterial pressure. Moreover, it has been established that at the same level of mean blood pressure, the observed target organ damage is also related to the variability of arterial pressure.3t *