Impaired responses of sympathetic nerves to cardiac receptor stimulation in hypertension.

Abstract

We recently reported that the vagal cardiopulmonary baroreceptor reflex inhibition of renal nerve traffic is impaired in rabbits with renal hypertension. The purpose of this study was to determine if the locus of the abnormality is mainly in the brain or in the afferent limb of the reflex. Experiments were done in alpha-chloralose-anesthetized rabbits with (n = 10) or without (n = 10) hypertension induced 6 to 8 weeks before study by wrapping the left kidney in cellophane followed by removal of the right kidney. The left side of the chest was opened, and a pericardial cradle was made. Nicotine was applied to the epicardial surface of the heart in concentrations of 10 to 500 micrograms/ml, and changes in arterial pressure and renal nerve traffic were measured. Dose-dependent decreases in traffic and arterial pressure resulted that were significantly smaller in hypertensive than in normotensive rabbits. After sinoaortic baroreceptor denervation, a similar impairment in the responses of hypertensive rabbits was observed. Vagotomy nearly abolished the responses of the renal nerves to epicardial nicotine. The responses of the lumbar sympathetic nerves to epicardial nicotine also were impaired in renal hypertensive (n = 8) compared with normotensive rabbits (n = 8). If the behavior and number of chemically sensitive endings are assumed to be unaltered in hypertension, then these findings are explained best by an abnormality in the central nervous system. These results support the view that the previously reported impairment in the vagal cardiopulmonary baroreceptor reflex control of renal nerve traffic is due mainly to a central abnormality, although they do not exclude an abnormality in the afferent limb of the reflex.