Fink G D, Bryan W J
Am J Physiol. 1980 Nov;239(5):F474-7. doi: 10.1152/ajprenal.1980.239.5.F474.
Increased sympathetic nervous system activity in the kidney has been postulated as a possible etiologic factor in some forms of hypertension. The present investigation sought to document the possibility of a chronic increase in neurogenic renal vasoconstriction in an experimental model in which increased nervous activity would be expected--neurogenic hypertension resulting from partial baroreceptor deafferentation. In anesthetized rats with chronic neurogenic hypertension, renal vascular resistance was significantly higher than in sham-operated rats. After acute renal denervation, there was no statistically significant difference in renal vascular resistance between the two groups. Thus, a chronic increase in neurogenic renal vascular resistance was apparent in the hypertensive rats. Since renal vascular responses to direct renal nerve activation, norepinephrine, and other exogenous vasoactive hormones were not altered in the hypertensive rats, the increased neurogenic vasoconstriction was probably the result of increased renal nerve discharge. Unaltered neurotransmission and reactivity further indicated a failure of the renal nerves or blood vessels to "adapt" to increased nervous activity. These results support previous suggestions that increased renal sympathetic nerve activity could result in sustained neurogenic renal vasoconstriction and thereby contribute to the development of hypertension.
肾脏交感神经系统活动增强被认为是某些类型高血压可能的病因。本研究旨在证实，在一个预期神经活动会增强的实验模型——部分压力感受器去传入神经导致的神经源性高血压中，神经源性肾血管收缩存在慢性增强的可能性。在患有慢性神经源性高血压的麻醉大鼠中，肾血管阻力显著高于假手术大鼠。急性肾去神经支配后，两组大鼠的肾血管阻力无统计学显著差异。因此，高血压大鼠中神经源性肾血管阻力存在慢性增强。由于高血压大鼠对直接肾神经激活、去甲肾上腺素和其他外源性血管活性激素的肾血管反应未改变，神经源性血管收缩增强可能是肾神经放电增加的结果。神经传递和反应性未改变进一步表明肾神经或血管未能对增加的神经活动“适应”。这些结果支持了先前的观点，即肾交感神经活动增加可导致持续性神经源性肾血管收缩，从而促进高血压的发展。
