Abildgaard U, Amtorp O, Agerskov K, Sjøntoft E, Christensen N J, Henriksen O
Circ Res. 1987 Aug;61(2):194-202. doi: 10.1161/01.res.61.2.194.
Blood flow studies were conducted in neurolept anesthetized dogs to characterize the involvement of renal nerves in ipsilateral renal vasoconstriction seen during acute elevation of renal venous pressure above 30 mm Hg. Renal blood flow was measured electromagnetically. The vasoconstrictor response was almost abolished by acute surgical denervation of the kidney, since renal vascular conductance remained unchanged during renal venous pressure elevation from 30-60 mm Hg. However, following additional alpha-adrenoceptor blockade or chronic renal denervation, renal vascular conductance increased progressively during renal venous pressure elevation to 60 mm Hg. The effect of acute decapsulation of kidney was studied in another group of dogs. Decapsulation induced a vasoconstriction. The decrease in renal vascular conductance observed during renal venous pressure elevation was unaffected by acute surgical denervation of decapsulated kidney, but was almost abolished following additional alpha-adrenoceptor blockade or chronic denervation. In decapsulated chronically denervated kidney, the increase in renal vascular conductance during renal venous pressure elevation to 60 mm Hg was still present but considerably attenuated as compared with the chronically denervated kidney with intact capsule. The renin-angiotensin system did not participate in acute vascular adjustments to renal venous stasis in intact kidney or in decapsulated acutely surgically denervated kidney. The data favor the view that neurogenic and myogenic mechanisms significantly influence the vasoconstrictor response to renal venous pressure elevation in dog kidney. The neurogenic contribution to the vasoconstrictor response comprises intrarenal and extrarenal vasoconstrictor mechanisms evoked reflexively by renal venous pressure elevation, and the myogenic contribution to the vasoconstrictor response comprises opposing vasodilator mechanisms due to increase in renal interstitial tissue pressure during renal venous pressure elevation.
在接受神经安定麻醉的犬身上进行血流研究，以确定在肾静脉压力急性升高至30 mmHg以上时，肾神经参与同侧肾血管收缩的情况。通过电磁法测量肾血流量。急性手术去神经支配肾脏后，血管收缩反应几乎消失，因为在肾静脉压力从30 mmHg升高至60 mmHg期间，肾血管传导率保持不变。然而，在额外给予α-肾上腺素能受体阻断或慢性肾去神经支配后，在肾静脉压力升高至60 mmHg期间，肾血管传导率逐渐增加。在另一组犬中研究了急性肾被膜剥脱的影响。被膜剥脱引起血管收缩。在肾静脉压力升高期间观察到的肾血管传导率降低不受急性手术去神经支配的被膜剥脱肾脏的影响，但在额外给予α-肾上腺素能受体阻断或慢性去神经支配后几乎消失。在被膜剥脱的慢性去神经支配肾脏中，在肾静脉压力升高至60 mmHg期间肾血管传导率的增加仍然存在，但与有完整被膜的慢性去神经支配肾脏相比明显减弱。肾素-血管紧张素系统不参与完整肾脏或急性手术去神经支配的被膜剥脱肾脏对肾静脉淤滞的急性血管调节。这些数据支持以下观点，即神经源性和肌源性机制显著影响犬肾对肾静脉压力升高的血管收缩反应。对血管收缩反应的神经源性贡献包括肾静脉压力升高反射性诱发的肾内和肾外血管收缩机制，而对血管收缩反应的肌源性贡献包括由于肾静脉压力升高期间肾间质组织压力增加而产生的相反的血管舒张机制。
