Denton K M, Li M, Anderson W P, Whitworth J A
Department of Physiology, Monash University, Melbourne, Australia.
J Hypertens. 2001 Feb;19(2):327-34. doi: 10.1097/00004872-200102000-00021.
To determine the effects on pre- and post-glomerular vascular resistance of adrenocorticotrophin (ACTH)-induced hypertension in rats, before and after blockade of nitric oxide formation.
Four groups of Sprague-Dawley rats were studied. Measurements were made in ACTH- (Synacthen Depot, 0.25 mg/kg twice daily for 8 days) and sham-treated anaesthetized rats, before and after either Nomega-nitro-L-arginine (L-NNA, 6 mg/kg) or vehicle.
Whole-kidney and single-nephron haemodynamics and function were measured. Glomerular capillary pressure was estimated from tubular stop-flow pressure measurements.
Blood pressure (P < 0.001), renal blood flow (RBF, P < 0.05) and glomerular filtration rate (P < 0.01) were increased following ACTH treatment compared with sham. There were no differences in either total renal, or pre- or post-glomerular vascular resistances, but stop-flow-estimated glomerular capillary pressure was elevated (P < 0.001) as was single-nephron glomerular filtration rate (SNGFR) (P < 0.001) and single-nephron blood flow (P < 0.01 ) in the ACTH- compared to the sham-treated rats. L-NNA treatment increased blood pressure by a similar extent in both ACTH- and sham-treated rats, but reduced RBF (P < 0.05) and glomerular filtration rate (GFR) (P < 0.05) more in the ACTH group; similar changes were seen in single-nephron values. L-NNA increased pre- and post-glomerular resistances to a greater extent in the ACTH group.
ACTH-induced hypertension produced glomerular hypertension and hyperfiltration, which may be due to nitric oxide-related vasodilatation of the renal vasculature.
确定在一氧化氮生成被阻断前后，促肾上腺皮质激素（ACTH）诱导的大鼠高血压对肾小球前和肾小球后血管阻力的影响。
对四组斯普拉格 - 道利大鼠进行研究。在给予ACTH（长效合成促肾上腺皮质激素，0.25mg/kg，每日两次，共8天）和假手术处理的麻醉大鼠中，于给予N-ω-硝基-L-精氨酸（L-NNA，6mg/kg）或溶剂前后进行测量。
测量全肾和单肾单位的血流动力学及功能。通过肾小管停流压力测量估算肾小球毛细血管压力。
与假手术组相比，ACTH处理后血压（P<0.001）、肾血流量（RBF，P<0.05）和肾小球滤过率（P<0.01）升高。总肾血管阻力、肾小球前或肾小球后血管阻力均无差异，但与假手术组相比，ACTH处理组中通过停流估算的肾小球毛细血管压力升高（P<0.001），单肾单位肾小球滤过率（SNGFR）（P<0.001）和单肾单位血流量（P<0.01）也升高。L-NNA处理使ACTH处理组和假手术处理组的血压升高幅度相似，但在ACTH组中对RBF（P<0.05）和肾小球滤过率（GFR）（P<0.05）的降低作用更大；单肾单位数值也出现类似变化。L-NNA在ACTH组中使肾小球前和肾小球后阻力升高的程度更大。
ACTH诱导的高血压导致肾小球高血压和超滤，这可能归因于肾血管系统中与一氧化氮相关的血管舒张。
