Sadowski J, Badzyńska B
Laboratory of Renal & Body Fluid Physiology, M. Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland.
J Physiol Pharmacol. 2006 Nov;57 Suppl 11:169-78.
The status of intrarenal circulation determines in part renal excretion, affects body fluid homeostasis and has a role in long term control of arterial blood pressure. The vascular resistance in the renal cortex and medulla is determined by interaction of a vast array of vasoactive hormones and paracrine factors; among these the role of constrictor angiotensin II and dilator prostaglandins and nitric oxide may appear to be dominating. The focus of this review and underlying studies is on the mechanisms whereby the microcirculation of the renal medulla is protected against the vasoconstrictor action of angiotensin II. In anaesthetized normal rats the three mentioned active agents or their inhibitors were applied and total renal blood flow and cortical, outer- and inner medullary laser-Doppler fluxes were determined; in some studies renal tissue nitric oxide was measured using selective electrodes. We conclude that angiotensin II, acting via AT1 receptors, constricts the renal cortical vasculature; in the medulla its action is effectively buffered by prostaglandin E2 but most probably not by nitric oxide.
肾内循环状态部分决定了肾脏排泄,影响体液平衡,并在动脉血压的长期控制中发挥作用。肾皮质和髓质的血管阻力由大量血管活性激素和旁分泌因子相互作用决定;其中,缩血管的血管紧张素II以及扩血管的前列腺素和一氧化氮的作用可能最为突出。本综述及相关基础研究的重点是肾髓质微循环免受血管紧张素II缩血管作用影响的机制。在麻醉的正常大鼠中,应用上述三种活性剂或其抑制剂,并测定总肾血流量以及皮质、外髓和内髓的激光多普勒血流;在一些研究中,使用选择性电极测量肾组织中的一氧化氮。我们得出结论,血管紧张素II通过AT1受体发挥作用,使肾皮质血管收缩;在髓质中,其作用可被前列腺素E2有效缓冲,但很可能不是由一氧化氮缓冲。