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心房利钠肽(ANP)输注期间大鼠的肾间质压力与肾小管-肾小球反馈控制

Renal interstitial pressure and tubuloglomerular feedback control in rats during infusion of atrial natriuretic peptide (ANP).

作者信息

Morsing P, Stenberg A, Casellas D, Mimran A, Müller-Suur C, Thorup C, Holm L, Persson A E

机构信息

Department of Physiology and Biophysics, University of Lund, Sweden.

出版信息

Acta Physiol Scand. 1992 Nov;146(3):393-8. doi: 10.1111/j.1748-1716.1992.tb09434.x.

DOI:10.1111/j.1748-1716.1992.tb09434.x
PMID:1481694
Abstract

Atrial natriuretic peptide (ANP), injected at physiological concentrations, is known to induce both natriuresis and diuresis. It has been suggested by some investigators that these changes result from an increasing glomerular filtration rate (GFR), but others have been unable to demonstrate an increased GFR. The tubuloglomerular feedback (TGF) mechanism is an important regulator of GFR, and the sensitivity of TGF is decreased during ANP administration. Furthermore, resetting of TGF is, in most instances, related to changes in renal interstitial hydrostatic and oncotic pressures. It is also known that ANP may increase capillary permeability which may change renal interstitial pressure. The present study was performed to examine renal interstitial pressures and the TGF mechanism during ANP infusion. In accordance with previous studies, TGF sensitivity was found to be decreased. The tubular flow rate which elicited half the maximal drop in stop-flow pressure (Psf) was increased from 18.5 to 25.7 nl min-1. In contrast, ANP infusion resulted in a decreased interstitial hydrostatic pressure and an increased interstitial oncotic pressure. From previous experiments, such changes in interstitial pressures would be expected to increase TGF sensitivity. The changes in interstitial pressure cannot, therefore, directly explain the resetting of the feedback mechanism. In conclusion, the present paper shows a decreased renal net interstitial pressure after intravenous administration of ANP.

摘要

注射生理浓度的心房利钠肽(ANP)已知可引起利钠和利尿作用。一些研究人员认为,这些变化是由肾小球滤过率(GFR)增加所致,但其他研究人员未能证明GFR增加。肾小管-肾小球反馈(TGF)机制是GFR的重要调节因子,在给予ANP期间TGF的敏感性降低。此外,在大多数情况下,TGF的重置与肾间质静水压和胶体渗透压的变化有关。还已知ANP可能增加毛细血管通透性,这可能改变肾间质压力。本研究旨在检查ANP输注期间的肾间质压力和TGF机制。与先前的研究一致,发现TGF敏感性降低。引起停流压力(Psf)最大下降一半的肾小管流速从18.5 nl min-1增加到25.7 nl min-1。相反,输注ANP导致间质静水压降低和间质胶体渗透压升高。根据先前的实验,预计间质压力的这种变化会增加TGF敏感性。因此,间质压力的变化不能直接解释反馈机制重置的原因。总之,本文显示静脉注射ANP后肾净间质压力降低。

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