Cardiac and vascular structural adaptation in experimental hypertension.

Various colonies of the spontaneously hypertensive rat (SHR) of the same age demonstrate different forms of the left ventricle (LV) in end-diastole. SHR from breeders in Australia and Switzerland exhibit concentrically hypertrophied LV, evident from an increased wall thickness to internal radius ratio (w/ri), while SHR from a Danish colony show an unchanged w/ri ratio, indicating eccentrically hypertrophied LV. These differences may be related to changes in arterial blood pressure and/or altered cardiac filling patterns. A more favourable situation seems to prevail for the eccentrically hypertrophied SHR heart compared with the concentrically hypertrophied heart, the former demonstrating enhanced cardiac function. Thus, an LV with increased diastolic diameter, as in the eccentrically hypertrophied SHR heart, can produce an elevated stroke volume for a given degree of myocardial shortening. In renal hypertension, however, LV function was depressed, probably due to a factor, possibly released upon clipping of the renal artery, that has inherent negative inotropic properties. Here, the reduction of LV performance could be explained neither by the changed LV geometrical design nor by the altered myocardial myosin isoenzyme pattern. At low aortic pressures and hence limited coronary perfusion, LV performance is attenuated in SHR and renal hypertensive rats, most likely due to the vascular structural changes within the coronary vascular bed.