Chen K, Zimmerman B G
Department of Pharmacology, University of Minnesota Medical School, Minneapolis 55455, USA.
Eur J Pharmacol. 1995 Sep 25;284(3):281-8. doi: 10.1016/0014-2999(95)00357-q.
Renal adrenergic interactions of intravenously and intrarenal arterially administered angiotensin II were studied in the anesthetized rabbit. Systemic arterial blood pressure and left renal blood flow were monitored. Bolus doses of angiotensin II, 50 and 100 ng/kg given intravenously, caused an immediate reduction in renal blood flow followed by a more sustained vasoconstrictor response. Prazosin, 5 micrograms/kg/min, infused intrarenal arterially, decreased both components of the reduced renal blood flow, suggesting adrenergic contribution to the response. Renal denervation reduced significantly the immediate response to angiotensin II without affecting the sustained response; administration of prazosin after denervation caused a further decrease in the response. Left adrenalectomy had no significant effect on the angiotensin II-induced renal blood flow response, ruling out the possible contribution of adrenal catecholamine release via the adrenal rete. In animals that had undergone renal denervation and left adrenalectomy, the renal blood flow response to intrarenal arterial injection of subpressor doses of angiotensin II (5 and 10 ng/kg) was reduced by the infusion of prazosin. It is concluded that angiotensin II-induced renal vasoconstriction is contributed to by adrenergic actions dependent in part on intact renal nerves, but also by a component not requiring an intact nerve supply.
在麻醉兔身上研究了静脉注射和肾动脉内注射血管紧张素II的肾肾上腺素能相互作用。监测全身动脉血压和左肾血流量。静脉注射50和100 ng/kg的血管紧张素II推注剂量，导致肾血流量立即减少，随后出现更持久的血管收缩反应。以5微克/千克/分钟的速度肾动脉内输注哌唑嗪，可降低肾血流量减少的两个组成部分，提示肾上腺素能对该反应有贡献。肾去神经支配显著降低了对血管紧张素II的即时反应，但不影响持续反应；去神经支配后给予哌唑嗪导致反应进一步降低。左肾上腺切除术对血管紧张素II诱导的肾血流量反应无显著影响，排除了通过肾上腺网释放肾上腺儿茶酚胺的可能贡献。在进行了肾去神经支配和左肾上腺切除术的动物中，肾动脉内注射低于升压剂量的血管紧张素II（5和10 ng/kg）引起的肾血流量反应因输注哌唑嗪而降低。结论是，血管紧张素II诱导的肾血管收缩部分依赖于完整的肾神经的肾上腺素能作用，但也有一部分不需要完整的神经供应。
