Absence of increase in left ventricular mass in dogs with bilateral renovascular hypertension.

Using sonomicrometric and indwelling pressure transducers, 16 healthy, normotensive dogs were prepared for semicontinuous monitoring of left ventricular (LV) mass, volumes, pressures, flows and wall tension (W Ten), aortic pressure (AP), total peripheral resistance (TPR), and indices of myocardial contractility. After a period of control measurements, bilateral renal artery constriction (2K-2C) was produced in 5 dogs and monitoring continued for 3 weeks or more. Mean arterial pressure (MAP) and LV end-systolic pressure (LVESP) was significantly higher (P less than 0.01) in the 2K-2C dogs compared to controls. There was no significant difference in LV mass, W Ten, or dP/dt, although TPR was 65% higher in the 2K-2C dogs. Comparable data from five dogs with single kidney hypertension (1K-1C), after 3 weeks, showed an elevated MAP and LVESP similar to the 2K-2C dogs. This group also showed a significant increase in LV mass and dP/dt (P less than 0.01), while the TPR was significantly decreased. The data suggest that the mechanism of hypertension development in the 2K-2C dog is different from that of the 1K-1C dog, and that there is evidence of increase in neuroadrenergic activity (viz, myocardial contractility) associated with the development of LV hypertrophy. The role of W Ten in the hypertrophic process was less clear from these data. Further study of these models may provide insight into the relative roles of the neuroadrenergic and volume-vasoconstriction components in the pathogenesis of hypertension and changes in LV mass.