HIGH NACL DIET ENHANCES ARTERIAL BARORECEPTOR REFLEX IN NACL-SENSITIVE SPONTANEOUSLY HYPERTENSIVE RATS

Previous studies from our laboratory have shown that arterial baroreceptor reflex control of lumbar sympathetic nerve activity is blunted in the NaCl-sensitive spontaneously hypertensive rat (SHR-S) compared with either the NaCl-resistant spontaneously hypertensive rat (SHR-R) or the normotensive Wistar-Kyoto (WKY) rat. In the current study, the effect of dietary NaCl supplementation on arterial baroreceptor reflex control of lumbar sympathetic nerve activity and heart rate was assessed in SHR-S and control SHR-R and WKY rats. Male SHR-S, SHR-R, and WKY rats were fed diets containing either 1% or 8% NaCl beginning at 7 weeks of age and were studied at age 9-10 weeks. Arterial baroreceptor reflex-mediated changes in lumbar sympathetic nerve activity and heart rate were recorded in conscious, unrestrained rats during phenylephrine-induced (15-40-mu-g/kg/min) and nitroprusside-induced (15-300-mu-g/kg/min) changes in mean arterial pressure. SHR-S maintained on a 1% NaCl diet had blunted baroreceptor reflex control of lumbar sympathetic nerve activity during acute increases in MAP compared with SHR-R and WKY rats (p < 0.05). After ingestion of the 8% NaCl diet, this blunting was absent, indicating enhancement of baroreceptor reflex control of lumbar sympathetic nerve activity. SHR-S maintained on a 1% NaCl diet also had blunted arterial baroreceptor control of lumbar sympathetic nerve activity during nitroprusside-induced decreases in mean arterial pressure compared with WKY rats, but this was not significantly altered during ingestion of the 8% NaCl diet. Arterial baroreceptor reflex-mediated control of heart rate during acute increases or decreases in MAP was blunted in SHR-S and SHR-R maintained on either diet compared with WKY rats (p < 0.05). The NaCl-induced augmentation of arterial baroreceptor reflex control of lumbar sympathetic nerve activity in SHR-S would serve to buffer the NaCl-induced increase in mean arterial pressure. Further study is needed to elucidate its mechanism.