Aldosterone reduces baroreceptor discharge in the dog.
Aldosterone reduces baroreceptor discharge in the dog.
复制标题
醛固酮减少狗的压力感受器放电。
DOI：
10.1161/01.hyp.19.3.270
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发表时间：
1992
期刊：
影响因子：
--
通讯作者：
Zucker,IH
中科院分区：
文献类型：
--
作者：
Wang,W;McClain,JM;Zucker,IH
我们之前已经证明，实验性心力衰竭狗的压力感受器放电敏感性降低，这种降低的敏感性可以通过Na+，K(+)- atp酶抑制剂瓦巴因逆转。这表明压力感受器中Na+，K(+)- atp酶活性的增强是心力衰竭状态下压力感受器放电敏感性减弱的原因。由于醛固酮（一种已知的Na+，K(+)- atp酶的刺激物）在心力衰竭时升高，本研究旨在确定在血压正常的狗颈动脉窦灌注醛固酮对压力感受器放电的影响。记录单个压力感受器活动、颈动脉窦压力和颈动脉窦直径。颈动脉窦灌注醛固酮（Krebs-Henseleit溶液）可显著提高阈压（108.5 +/- 3.1 mm Hg vs 92.7 +/- 4.6 mm Hg, p < 0.05），降低峰值放电率（40.3 +/- 3.9 spike /sec, p < 0.05）。这些效果在醛固酮灌注15分钟后出现，并在接下来的60分钟内保持不变。醛固酮灌注后颈动脉窦压径曲线无明显变化。在醛固酮灌注期间，用瓦巴因（0.1微克/毫升）灌注颈动脉窦不能逆转钝化的压力感受器放电。颈动脉窦内灌注醛固酮引起的压力感受器活性钝化可通过球囊导管去除颈动脉窦内内皮细胞或灌注皂苷来预防。最后，在颈动脉窦内灌注10 ng/ml的螺内酯（一种矿物皮质激素受体拮抗剂）可以阻止醛固酮的抑制作用。这些数据表明醛固酮降低压力感受器最大放电。（摘要删节250字）
We have previously demonstrated that baroreceptor discharge sensitivity is depressed in dogs with experimental heart failure and that this depressed sensitivity can be reversed by the Na+,K(+)-ATPase inhibitor ouabain. This suggests that enhanced Na+,K(+)-ATPase activity in baroreceptors is responsible for the blunted baroreceptor discharge sensitivity seen in heart failure state. Because aldosterone, a known stimulator of Na+,K(+)-ATPase, is elevated in heart failure the present study was undertaken to determine the effects on baroreceptor discharge of perfusion of the carotid sinus with aldosterone in normotensive dogs. Single unit baroreceptor activity was recorded as well as carotid sinus pressure and the diameter of the carotid sinus. Perfusion of the carotid sinus with aldosterone (in Krebs-Henseleit solution) significantly elevated threshold pressure (108.5 +/- 3.1 mm Hg versus 92.7 +/- 4.6 mm Hg, p less than 0.05) and reduced peak discharge rate (40.3 +/- 3.9 spikes/sec, p less than 0.05). These effects appeared 15 minutes after aldosterone perfusion and remained constant for the next 60 minutes. There was no change in the carotid sinus pressure-diameter curve during perfusion with aldosterone. Perfusion of the carotid sinus with ouabain (0.1 microgram/ml) during aldosterone perfusion did not reverse the blunted baroreceptor discharge. The blunted baroreceptor activity induced by perfusion of the carotid sinus with aldosterone was prevented by removal of the endothelial cells in the carotid sinus area with a balloon-tipped catheter or by perfusion with saponin. Finally, perfusion of the carotid sinus with spironolactone (10 ng/ml), a mineralocorticoid receptor antagonist, prevented the inhibitory effect of aldosterone. These data suggest that aldosterone reduces maximum baroreceptor discharge.(ABSTRACT TRUNCATED AT 250 WORDS)