Zambraski E J, Dibona G F, Kaloyanides G J
J Pharmacol Exp Ther. 1976 Aug;198(2):464-72.
To evaluate the effects of reflex renal sympathetic nerve stimulation on renal tubular sodium handling, clearance studies were performed in anesthetized dogs. With renal perfusion pressure held constant, baroreceptor reflex renal sympathetic nerve stimulation was produced by controlled arterial hemorrhage or carotid sinus perfusion. Significant decreases in urinary sodium excretion occurred in the presence of minor insignificant alterations in renal blood flow and no changes in glomerular filtration rate. Renal alpha adrenergic receptor blockade (phenoxybenzamine) or adrenergic blockade (guanethidine) completely reversed the fall in urinary sodium excretion; this could not be attributed to alterations in glomerular filtration rate or renal blood flow. These studies support the interpretation that adrenergic innervation of the renal tubules is involved in the regulation of renal tubular sodium reabsorption.
为评估反射性肾交感神经刺激对肾小管钠处理的影响,在麻醉犬身上进行了清除率研究。在肾灌注压保持恒定的情况下,通过控制性动脉出血或颈动脉窦灌注产生压力感受器反射性肾交感神经刺激。在肾血流量仅有轻微无显著意义改变且肾小球滤过率无变化的情况下,尿钠排泄显著减少。肾α肾上腺素能受体阻断(酚苄明)或肾上腺素能阻断(胍乙啶)完全逆转了尿钠排泄的下降;这不能归因于肾小球滤过率或肾血流量的改变。这些研究支持以下解释,即肾小管的肾上腺素能神经支配参与肾小管钠重吸收的调节。