de Matteo R, May C N
Howard Florey Institute of Experimental Physiology and Medicine, University of Melbourne, Parkville 3052, Australia.
Am J Physiol. 1999 Apr;276(4):R1125-31. doi: 10.1152/ajpregu.1999.276.4.R1125.
Glucocorticoids increase renal blood flow (RBF) and glomerular filtration rate in many species, but the mechanisms involved are unclear. We investigated whether cortisol-induced renal vasodilatation in conscious sheep depends on interactions with prostaglandins or angiotensin II. Intravenous infusion of cortisol (5 mg/h) for 5 h increased renal conductance (RC) by 1.06 +/- 0.24 ml. min-1. mmHg-1 more than vehicle. During intrarenal infusion of indomethacin (0.25 mg. kg-1. h-1), the cortisol-induced increase in RC (0.28 +/- 0.21 ml. min-1. mmHg-1) was significantly reduced. The cortisol-induced rise in RBF (103 +/- 17 ml/min) was not significantly reduced by indomethacin treatment (76 +/- 9 ml/min). Combined intrarenal infusion of indomethacin (0.25 mg. kg-1. h-1) with Nomega-nitro-L-arginine (2.0 mg. kg-1. h-1), a nitric oxide synthase inhibitor, abolished the cortisol-induced increases in both RC and RBF. Inhibition of angiotensin II synthesis with intravenous captopril (40 mg/h) blocked the renal vasoconstrictor action of angiotensin I but did not inhibit the cortisol-induced increases in RBF and RC. This study provides evidence that nitric oxide and prostaglandins play a role in cortisol-induced renal vasodilatation but indicates that this response is independent of an interaction with angiotensin.
糖皮质激素可增加多种物种的肾血流量（RBF）和肾小球滤过率，但其涉及的机制尚不清楚。我们研究了皮质醇诱导清醒绵羊肾血管舒张是否依赖于与前列腺素或血管紧张素II的相互作用。静脉输注皮质醇（5mg/h）5小时使肾电导（RC）比输注溶媒时增加了1.06±0.24ml·min⁻¹·mmHg⁻¹。在肾内输注吲哚美辛（0.25mg·kg⁻¹·h⁻¹）期间，皮质醇诱导的RC增加（0.28±0.21ml·min⁻¹·mmHg⁻¹）显著降低。吲哚美辛治疗（76±9ml/min）并未显著降低皮质醇诱导的RBF升高（103±17ml/min）。肾内联合输注吲哚美辛（0.25mg·kg⁻¹·h⁻¹）和一氧化氮合酶抑制剂Nω-硝基-L-精氨酸（2.0mg·kg⁻¹·h⁻¹）消除了皮质醇诱导的RC和RBF增加。静脉注射卡托普利（40mg/h）抑制血管紧张素II合成可阻断血管紧张素I的肾血管收缩作用，但不抑制皮质醇诱导的RBF和RC增加。本研究提供了证据表明一氧化氮和前列腺素在皮质醇诱导的肾血管舒张中起作用，但表明这种反应独立于与血管紧张素的相互作用。
