Renal denervation normalizes pressure and baroreceptor reflex in high renin hypertension in conscious rats

Abstract

High renin hypertension is usually accompanied by impairment of the baroreceptor reflexes. This feature has been mostly ascribed to overactivity of the renin-angiotensin system. However, renal nerves could also modulate the baroreceptor reflexes. In the present experiments, the effect of renal denervation on the depressed baroreceptor reflexes was studied in rats subjected to aortic ligation between the renal arteries. Renal denervation of the ischemic kidney was performed at the same time as aortic ligation. The resulting effects on arterial pressure, heart rate, plasma renin activity, and baroreceptor reflex control of heart rate were studied 10–12 days after ligation and denervation. Aortic ligation induced high levels of mean arterial pressure (166±6 versus 110±3 mm Hg in controls), heart rate (380±9 versus 352±8 beats per minute in controls), and plasma renin activity (44±5 versus 6±1.2 ng angiotensin I/ml/hr). The baroreceptor reflex sensitivity for bradycardia and tachycardia was significantly reduced (−0.18±0.04 and −0.18±0.05, respectively, versus −2.3±0.01 and −2.4±0.1 beats per minute per mm Hg in controls). Denervation of the ischemic kidney attenuated the development of hypertension in aortic-ligated rats (122±3 mm Hg), lowering heart rate (319±8 beats per minute) and normalizing baroreceptor reflex sensitivity to bradycardia (−2.0±0.2 beats per minute per mm Hg) and to tachycardia (−4.0±0.1 beats per minute per mm Hg). Plasma renin activity was also normalized (4.3±2.4 ng angiotensin I/ml/hr). Baroreceptor reflex sensitivity assessed 10 days after unilateral renal denervation in three control rats showed no alteration when compared with baroreceptor reflex sensitivity assessed before denervation in the same rat Because normalization of the baroreceptor reflexes after complete renal denervation was accompanied also by normalization of plasma renin activity, this effect could be mostly explained by the well-known action of angiotensin II on baroreceptor reflex function. © 1992 American Heart Association, Inc.