Echtenkamp S F, Anderson A C
Department of Physiology and Biophysics, Indiana University School of Medicine, Gary 46408.
Am J Physiol. 1988 May;254(5 Pt 2):H905-11. doi: 10.1152/ajpheart.1988.254.5.H905.
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.
慢性钠缺失与压力感受性反射对颈动脉窦低血压的反应性降低有关。一种解释压力感受性反射反应性降低机制的假说是，钠缺失期间血容量会重新分布至心肺循环。这种容量重新分布可能导致心肺容量感应机械感受器的放电增加，从而持续抑制颈动脉压力感受性反射的表达。在本研究中，当测试对颈动脉闭塞的升压和心动过速反应时，钠缺失犬的压力感受性反射反应明显较小（P<0.05）。当切断迷走神经和主动脉减压神经后，钠充足和钠缺失动物对颈动脉闭塞的压力感受性反射反应均增强。然而，迷走神经切断术后，钠缺失动物的升压和心动过速反应仍减弱（P<0.05）。因此，本研究结果表明，钠缺失状态下心肺容量感受器放电并未增加，去除心肺迷走神经传入影响并不能使钠缺失动物受损的压力感受性反射反应性恢复正常。
