Cardiac Output and Peripheral Resistance in Experimental Renal Hypertension

By means of an implanted electromagnetic flowmeter and an abdominal aortic cannula cardiac output and mean arterial blood pressure have been measured in unanesthetized rats subjected to the operation of left nephrectomy and the application of a clip to the right renal artery.

The hemodynamic changes occurring in a group of animals bearing a narrow clip and developing hypertension were compared with those in a group bearing a wide clip and remaining normotensive.

The cardiac output fell slightly in the first 3 days after operation in the hypertensive group, during which time the heart rate was depressed. As the heart rate rose again, the cardiac output increased and from the sixth day to the end of the observation period of 28 days the cardiac output in the hypertensive group exceeded that in the normotensive group by an average of 10%. At any one time the differences between the groups were not significant, but the differences were consistent and overall were significant at the P < 0.05 level. This increase in cardiac output was roughly attributable to equal increases in heart rate and stroke volume.

The change in stroke volume in the hypertensive group consistently exceeded that in the normotensive group, except over the eighth to ninth day, at which point the peak increase in heart rate occurred.

The peripheral resistance rose by an average of 30% within 2 hours of operation. Subsequently further increments occurred, and the raised blood pressure at all stages was mainly attributable to an increase in peripheral resistance. However, large fluctuations occurred and, in individual animals, increases in cardiac output were at times responsible for the hypertension.

When renal infarction occurred, large reductions in cardiac output and increases in calculated peripheral resistance took place. In one animal with partial renal infarction the hypertension followed a malignant course and the cardiac output was depressed until terminally.

In a separate experiment the arterial hematocrit was measured serially in a group of hypertensive and normotensive rats. In both groups the hematocrit fell after operation and then gradually returned to its original level. The fall was greater in the hypertensive group but after 11 days the difference was no greater than 0.5%.

These hemodynamic changes have been discussed in relation to possible pathogenetic mechanisms during the development and maintenance of benign experimental renal hypertension.