Abildgaard U
Department of Cardiology, Gentofte Hospital.
Dan Med Bull. 1989 Jun;36(3):212-22.
The effect of renal venous pressure (RVP) elevation on renal hemodynamics and tubular function was studied in neurolept anaesthetized dogs. Renal blood flow (RBF) was measured electromagnetically. Clearance of 51Cr-EDTA was used as a measure of the rate of glomerular filtration (GFR). GFR, urinary excretion rates of sodium and water, and lithium clearance (CLi) were used for assessing the absolute and fractional reabsorption rates of sodium and water in the proximal as well as in more distal segments of the nephron. The vasoconstrictor response to RVP elevation was partly abolished by acute surgical denervation or by local application of lidocain on the renal capsule, suggesting that RVP elevation activates an adrenergic vasoconstrictor reflex comprising the spinal cord, and elicited from stretch receptors located in the renal capsule. Further studies in alpha-adrenoceptor blocked or chronic denervated kidneys and in decapsulated kidneys favour the view, that neurogenic and myogenic mechanisms significantly influence the vasoconstrictor response to RVP elevation: The neurogenic contribution to the vasoconstrictor response comprising intrarenal and extrarenal vasoconstrictor mechanisms evoked reflexly by RVP elevation; the myogenic contribution to the vasoconstrictor response comprising opposing vasodilator mechanisms due to increase in renal interstitial tissue pressure during RVP elevation. Studies carried out in intact kidneys, acutely surgically or chronically denervated kidneys or alpha-adrenoceptor blocked kidneys indicate that the increase in proximal reabsorption rates during moderate RVP elevation is due mainly to local intrarenal alpha-adrenergic reflex mechanisms, since the decrease in CLi (during constant filtered load) induced by RVP elevation was unaffected by acute surgical denervation, but completely abolished by chronic denervation of the kidney, or by local alpha-adrenoceptor blockade of the kidney.
在神经安定麻醉的犬身上研究了肾静脉压（RVP）升高对肾血流动力学和肾小管功能的影响。用电磁法测量肾血流量（RBF）。51Cr - EDTA清除率用作肾小球滤过率（GFR）的指标。GFR、钠和水的尿排泄率以及锂清除率（CLi）用于评估近端以及肾单位更远端节段中钠和水的绝对重吸收率和分数重吸收率。急性手术去神经支配或在肾包膜局部应用利多卡因可部分消除对RVP升高的血管收缩反应，这表明RVP升高激活了一种包含脊髓的肾上腺素能血管收缩反射，该反射由位于肾包膜的牵张感受器引发。对α - 肾上腺素能受体阻断或慢性去神经支配的肾脏以及去包膜肾脏的进一步研究支持以下观点，即神经源性和肌源性机制显著影响对RVP升高的血管收缩反应：神经源性对血管收缩反应的贡献包括由RVP升高反射性诱发的肾内和肾外血管收缩机制；肌源性对血管收缩反应的贡献包括由于RVP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。在完整肾脏、急性手术或慢性去神经支配的肾脏或α - 肾上腺素能受体阻断的肾脏中进行的研究表明，在中度RVP升高期间近端重吸收率的增加主要归因于局部肾内α - 肾上腺素能反射机制，因为RVP升高（在恒定滤过负荷期间）引起的CLi降低不受急性手术去神经支配的影响，但可通过肾脏的慢性去神经支配或肾脏的局部α - 肾上腺素能受体阻断完全消除。
