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肾髓质血浆流速以及内髓集合管对盐和水的重吸收

Renal medullary plasma flow rate and reabsorption of salt and water from inner medullary collecting duct.

作者信息

Cupples W A, Sonnenberg H

机构信息

Department of Physiology, University of Toronto, Ont., Canada.

出版信息

Can J Physiol Pharmacol. 1987 Dec;65(12):2415-21. doi: 10.1139/y87-383.

DOI:10.1139/y87-383
PMID:3329570
Abstract

It has been proposed that medullary washout secondary to increased blood flow will limit maximal urine osmolality and reabsorption of salt and water from the inner medullary collecting duct. We have tested this prediction. The function of the inner medullary collecting duct was examined by microcatheterization. Acetylcholine was infused directly into the renal circulation, captopril was infused intravenously, and angiotensin II was infused into the renal circulation in rats which also received captopril. Medullary plasma flow rate, measured by dye-dilution in parallel experiments, was not significantly increased by acetylcholine; it was increased 30% (p less than 0.02) by systemic infusion of captopril, and was returned to control by angiotensin II. Acetylcholine increased both urine flow rate and sodium excretion (p less than 0.01, p less than 0.001, respectively), while captopril increased only sodium excretion (p less than 0.025). Angiotensin II blocked the natriuresis due to captopril. None of the treatments altered urine osmolality (p greater than 0.4 in all cases). Acetylcholine increased the loads of water, sodium, chloride, and total solute delivered to the inner medullary collecting duct. Angiotensin II reduced delivery of water and solutes compared with captopril alone. None of the treatments affected load dependency of reabsorption of water, sodium, chloride, or total solute in the inner medullary collecting duct. We conclude that there is, at most, a weak interaction between medullary blood flow and reabsorption from the inner medullary collecting duct.

摘要

有人提出,继发于血流量增加的髓质冲洗会限制最大尿渗透压以及内髓集合管对盐和水的重吸收。我们对这一预测进行了验证。通过微导管插入术检查内髓集合管的功能。在大鼠中,将乙酰胆碱直接注入肾循环,静脉注射卡托普利,并在同时接受卡托普利的大鼠中将血管紧张素II注入肾循环。在平行实验中通过染料稀释法测量的髓质血浆流速,乙酰胆碱未使其显著增加;全身注射卡托普利使其增加了30%(p<0.02),而血管紧张素II使其恢复到对照水平。乙酰胆碱增加了尿流率和钠排泄量(分别为p<0.01,p<0.001),而卡托普利仅增加了钠排泄量(p<0.025)。血管紧张素II阻断了卡托普利引起的利钠作用。所有处理均未改变尿渗透压(所有情况下p>0.4)。乙酰胆碱增加了输送到内髓集合管的水、钠、氯和总溶质的负荷。与单独使用卡托普利相比,血管紧张素II减少了水和溶质的输送。所有处理均未影响内髓集合管中水、钠、氯或总溶质重吸收的负荷依赖性。我们得出结论,髓质血流量与内髓集合管重吸收之间至多存在微弱的相互作用。

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