Baroreflex modulation by cardiopulmonary receptors during chronic sodium depletion.

Abstract

Chronic sodium to depletion is associated with a reduced baroreflex responsiveness to carotid sinus hypotension. One hypothesis to explain the mechanism of the reduced baroreflex responsiveness involves a redistribution of blood volume toward the cardiopulmonary circulation during sodium depletion. This volume redistribution may result in enhanced discharge of cardiopulmonary volume-sensing mechanoreceptors, which tonically inhibit the expression of the carotid baroreflex. In this study, when the pressor and tachycardic responses to carotid occlusion were tested, the baroreflex responses were significantly smaller in sodium-depleted dogs (P less than 0.05). When the vagal and aortic depressor nerves were removed, the baroreflex responses to carotid occlusion were increased in both sodium-replete and sodium-depleted animals. However, the pressor and tachycardic responses were still attenuated in the sodium-depleted animals after vagotomy (P less than 0.05). Thus the results of this study indicate that cardiopulmonary volume receptor discharge is not increased in the sodium-depleted state, and removal of cardiopulmonary vagal afferent influences does not normalize the impaired baroreflex responsiveness of sodium-depleted animals.