Reversal of experimental renovascular hypertension in the rat.

The experiments in this thesis were designed to examine the effects of surgical reversal of 2-kidney, 1-clip hypertension on baroreflexes and vascular capacitance. In the first set of experiments, baroreflex function was studied using a 'steady state' technique in conscious early phase 2-kidney, 1-clip rats before and 24 hours after surgical reversal of hypertension by unclipping or after pharmacological reduction of blood pressure by an infusion of hydralazine or captopril. A further group was studied 3 weeks after unclipping. With reduction of the blood pressure, the baroreflex was reset within 24 hours, irrespective of the method of blood pressure reduction, the degree of resetting being dependant on the level of blood pressure achieved. This resetting occurs without a change in baroreflex sensitivity. However, at 3 weeks after unclipping, the baroreflex sensitivity had returned to normal. In the second set of experiments, vascular capacitance was studied in conscious 2-kidney, 1-clip hypertensive rats and sham-clipped controls. Two further groups of 2-kidney, 1-clip rats were studied before and 6 hours after unclipping or a sham operation. Mean circulatory filling pressure (MCFP) was measured during a brief circulatory arrest by inflation of a right atrial balloon. Blood volume (BV) was measured by a radioisotopic dilution method and vascular compliance derived from the MCFP-BV curve. There was reduced vascular capacity in 2-kidney, 1-clip hypertension. Within 6 hours of unclipping, there was a marked reduction in mean circulatory filling pressure, with no change in blood volume or compliance, indicting a rapid increase in vascular capacity and reduction in venous tone. The third set of experiments explored the possible contribution of the renomedullary vasodepressor mechanisms to changes in vascular capacitance The model of chemical renal medullary damage secondary to bromoethylamine was used. In this study no difference in vascular capacitance was demonstrated, suggesting the lack of renomedullary vasodepressor mechanisms in the long-term had no demonstrable effect on venous tone.