Central effect of intravenous phenylephrine on baroreflex control of renal nerves

Responses of renal sympathetic nerve activity were determined in eight chloralose-anesthetized rabbits during sustained (1-3 minutes) increases in arterial pressure induced by phenylephrine infusion, and as arterial pressure returned to control. In four of the eight experiments, aortic baroreceptor traffic was also recorded. When arterial pressure was raised from 81 +/- 5 to 110 +/- 7 mm Hg, renal nerve activity decreased from 30 +/- 7 to 1 +/- 1 imp/sec. Aortic nerve activity increased from 208 +/- 35 to 346 +/- 49 imp/sec. When pressure returned to control (81 +/- 5 mm Hg), renal nerve activity remained inhibited (7 +/- 2 imp/sec), even though aortic nerve activity had also returned to control (195 +/- 33 imp/sec). Arterial pressure and traffic in the renal and aortic nerves returned to control over the succeeding 1 to 5 minutes. Transient increases in arterial pressure (lasting less than 1 minute) due to bolus injections of phenylephrine resulted in inhibition of renal nerve traffic followed by rapid recovery. In five rabbits with aortic and vagal nerves sectioned and both carotid sinuses isolated from the circulation, intravenous phenylephrine infusion augmented the gain of the isolated carotid baroreflex (particularly at low carotid sinus pressures). In nine experiments, injection of phenylephrine (0.01, 0.1, or 1.0 microgram) into the lateral ventricles did not change the basal renal nerve traffic but augmented the gain of the baroreflex control of the renal nerves. Our data indicate that peripherally infused phenylephrine can alter the arterial baroreflex control of the renal nerves by a central effect. The similar influence of intracerebroventricular phenylephrine on baroreflex control of the renal nerves is consistent with this view.