The Role of Endogenous Angiotensin II in Antidiuresis and Norepinephrine Overflow Induced by Stimulation of Renal Nerves in Anesthetized Dogs
The Role of Endogenous Angiotensin II in Antidiuresis and Norepinephrine Overflow Induced by Stimulation of Renal Nerves in Anesthetized Dogs
复制标题
内源性血管紧张素 II 在麻醉犬肾神经刺激引起的抗利尿和去甲肾上腺素溢出中的作用
DOI：
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发表时间：
1991
影响因子：
3
通讯作者：
S. Morimoto
中科院分区：
文献类型：
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作者：
K. Hayashi;Y. Matsumura;Y. Yoshida;Yasunori Suzuki;S. Morimoto
总结：我们研究了内源性血管紧张素II（ANG II）可能参与肾神经刺激（RNS）引起的去甲肾上腺素（NE）溢出和抗利尿作用。频率为0.5- 2.0Hz的RNS不影响肾血流动力学，但使尿流量和尿钠排泄量明显减少，NE分泌率（NESR）和肾素分泌率（RSR）升高。肾内动脉（i.r.a.）输入酚妥拉明（10 μg/kg/min）可消除RNS诱导的抗利尿作用。在接受卡托普利（15 μg/kg/min i. v.）的犬中，RNS诱导的抗利尿作用和NESR增加显著减弱。爱尔兰共和军以5 μg/kg/min的剂量给予普萘洛尔（完全抑制RNS引起的RSR增加的剂量），不影响RNS引起的NESR和尿形成的改变。在ANG II输注（1 ng/kg/min i.r.a.）期间，RNS导致尿液形成减少和NESR增加，幅度与未输注ANG II时相似。这些结果表明，RNS在低频率增加NESR和RSR不影响肾血流动力学和抗利尿作用可能是通过激活突触后α-肾上腺素受体，但不是通过ANG II受体，位于肾小管。NE的释放似乎是由ANG II通过激活易化的连接前机制来调节的，该机制最大限度地受到内源性和局部产生的ANG II基础水平的刺激。
Summary: We examined the possible involvement of endogenous angiotensin II (ANG II) in norepinephrine (NE) overflow and antidiuresis induced by renal nerve stimulation (RNS). RNS at a frequency of 0.5–2.0 Hz, which did not influence renal hemodynamics, produced significant reductions in urine flow and urinary excretion of sodium, and elevations in NE secretion rate (NESR) and renin secretion rate (RSR). Intrarenal arterial (i.r.a.) in-fusion of phentolamine (10 μg/kg/min) abolished the RNS-induced antidiuresis. In dogs receiving captopril (15 μg/kg/min i.v.), RNS-induced antidiuresis and increase in NESR were significantly attenuated. The i.r.a. administration of propranolol at 5 μg/kg/min, a dose that inhibited completely the RNS-induced increase in RSR, did not influence the alterations in NESR and urine formation in response to RNS. During ANG II infusion (1 ng/kg/min i.r.a.), RNS produced a reduction in urine formation and an increase in NESR, at a magnitude similar to that seen without ANG II infusion. These results suggest that RNS at a low frequency increased the NESR and RSR without affecting renal hemodynamics and that the antidiuretic effect was probably produced via the activation of postsynaptic a-adrenoceptors, but not via the ANG II receptor, located on the renal tubules. The release of NE appears to be modulated by ANG II through the activation of a facilitatory prejunctional mechanism, which is maximally stimulated by endogenously and locally generated basal levels of ANG II.