Role of renal alpha-adrenoceptors mediating renin secretion.
Role of renal alpha-adrenoceptors mediating renin secretion.
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肾α-肾上腺素受体介导肾素分泌的作用。
DOI：
10.1152/ajprenal.1982.242.6.f620
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发表时间：
1982
期刊：
影响因子：
--
通讯作者：
M. Thames
中科院分区：
文献类型：
--
作者：
J. Osborn;G. Dibona;M. Thames
低频率肾神经刺激（0.5 Hz）引起的肾素分泌增加发生在尿钠排泄或肾血流量没有变化的情况下，显然是来自肾交感神经对肾小球颗粒细胞的直接影响。我们试图确定肾α-肾上腺素受体在神经诱发的肾素分泌中的作用。用酚妥拉明或哌唑嗪阻断肾α-肾上腺素能受体不影响神经诱发的肾素分泌;然而，两个剂量水平的酚苄明同样抑制了肾素分泌。肾血管收缩反应分级肾神经刺激同样减少酚妥拉明，哌唑嗪，和较高的酚苄明剂量，而较低的酚苄明剂量是显着不太有效。甲氧胺在改变肾血流量和尿钠排泄的阈下剂量或仅减少尿钠排泄的剂量下输注刺激肾α肾上腺素受体也不改变肾素分泌。较高剂量的甲氧胺，减少肾血流量和钠排泄增加肾素分泌。基于酚妥拉明和哌唑嗪不能阻止神经介导的肾素分泌，以及甲氧胺与肾素分泌、肾血流量和尿钠排泄变化之间的剂量-反应关系，我们得出结论，肾α-肾上腺素受体不介导由肾小球颗粒细胞的直接神经激活引起的肾素分泌。这些数据表明，酚苄明抑制神经介导的肾素分泌的机制以外的肾α-肾上腺素受体阻滞。
The increase in renin secretion resulting from low-frequency renal nerve stimulation (0.5 Hz) occurs in the absence of changes in urinary sodium excretion or renal blood flow and is apparently derived from a direct effect of renal sympathetic nerves on juxtaglomerular granular cells. We sought to determine the role of renal alpha-adrenoceptors in this neurally evoked renin secretion. The neurally evoked renin secretion was unaffected by renal alpha-adrenoceptor blockade with phentolamine or prazosin; however, two dose levels of phenoxybenzamine equally inhibited the renin secretion. The renal vasoconstrictor response to graded renal nerve stimulation was similarly diminished by phentolamine, prazosin, and the higher phenoxybenzamine dose, whereas the lower phenoxybenzamine dose was significantly less effective. Renal alpha-adrenoceptor stimulation with methoxamine infusion at doses that were just subthreshold for altering renal blood flow and urinary sodium excretion or at doses that just reduced urinary sodium excretion also did not change renin secretion. Higher doses of methoxamine that decreased both renal blood flow and sodium excretion increased renin secretion. Based on the inability of phentolamine and prazosin to prevent neurally mediated renin secretion and on the dose-response relationship between methoxamine and changes in renin secretion, renal blood flow, and urinary sodium excretion, we conclude that renal alpha-adrenoceptors do not mediate renin secretion elicited by direct neural activation of the juxtaglomerular granular cells. The data suggest that phenoxybenzamine inhibits neurally mediated renin secretion by a mechanism other than renal alpha-adrenoceptor blockade.