Laboratory Investigation

Kidney International (1985) 27, 17–24; doi:10.1038/ki.1985.4

Influence of systemically applied angiotensin II on the microcirculation of glomerular capillaries in the rat

Bernd Zimmerhackl1, Niranjan Parekh1, Helmut Kücherer1 and Michael Steinhausen1

1I. Physiologisches Institut der Universität Heidelberg, Heidelberg, Federal Republic of Germany

Correspondence: Prof Dr M Steinhausen, I. Physiologisches Institut, Universität Heidelberg, Im Neuenheimer Feld 326, D-6900 Heidelberg, Federal Republic of Germany

Received 27 September 1982; Revised 23 January 1984.

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Abstract

Influence of systemically applied angiotensin II on the microcirculation of glomerular capillaries in the rat. The effect of intravenous infusion of angiotensin II on microvascular parameters of the renal microcirculation of rats was studied. With the aid of fluorescence microscopy and a high sensitivity video system we observed the passage of fluorescence-labeled erythrocytes through single glomerular capillaries on the surface of the rat kidney. From videotaped recordings, we measured the velocity and the flux of erythrocytes using a modified dual-slit technique with support of a microprocessor system. Angiotensin II was administered intravenously at a rate of either 0.2 or 0.4 microg/min/kg of body wt. Angiotensin II decreased renal blood flow in a dose-dependent fashion (a 32% decrease with 0.2 microg/min/kg and a 42% decrease with 0.4 microg/min/kg). The higher rate of angiotensin II infusion had a variable effect on red cell velocity in glomerular capillaries with an overall effect to decrease velocity by 18%. Red cell flux in capillaries was similarly decreased by 25% with angiotensin II infusion. Three successive infusions of angiotensin II did not significantly diminish the effect of the peptide on red cell velocity or flux. Volume flow through the glomerular capillaries (calculated from erythrocyte velocity and vessel diameter) decreased during angiotensin II infusion (0.4 microg/min/kg) from 3.2 to 2.4 nl/min despite no change in capillary diameter or hematocrit (ratio of erythrocyte flux to volume flow). These data indicate that alterations of the ultrafiltration coefficient (Kf) are not induced by uniform capillary vasoconstriction mechanisms, as others have suggested.

Influence de l'angiotensine II administrée par voie systémique sur la microcirculation des capillaires glomérulaires chez le rat. L'effet d'une perfusion intra-veineuse d'angiotensine II sur les paramètres microvasculaires de la microcirculation rénale de rats a été étudié. A l'aide de la microscopie par fluorescence et d'un système vidéo à haute sensibilité, nous avons observé le passage d'érythrocytes marqués par fluorescence à travers les capillaires glomérulaires individuels de la surface du rein de rat. A partir des enregistrements sur bandes vidéo, nous avons mesuré la vélocité et le flux des érythrocytes en utilisant une technique modifiée à double fente à l'aide d'un système à microprocesseur. L'angiotensine II était administrée par voie intra-veineuse à la vitesse de 0,2 ou 0,4 microg/min/kg de poids de corps. L'angiotensine II a diminué le débit sanguin rénale d'une façon dose dépendante (diminution de 32% avec 0,2 microg/min/kg et diminution de 42% avec 0,4 microg/min/kg). Le plus fort débit de perfusion d'angiotensine II avait un effet global de diminution de la vélocité de 18%; le flux de globules rouges dans les capillaries était diminué de la même façon de 25% par la perfusion d'angiotensine II. Trois perfusions successives d'angiotensine II n'ont pas diminué significativement l'effet du peptide sur la vélocité ou le flux des globules rouges. Le débit volumique à travers les capillaires glomérulaires (calculé à partir de la vélocité érythrocytaire et du diamètre des vaisseaux) a diminué pendant la perfusion d'angiotensine II (0,4 microg/min/kg) de 3,2 à 2,4 nl/min malgré l'absence de modification du diamètre capillaire, ou de l'hématocrite (rapport du flux érythrocytaire au débit volumique). Ces données indiquent que des altérations du coefficient d'ultrafiltration (Kf) ne sont pas induites par des mécanismes de vasoconstriction capillaire uniformes, comme d'autres l'ont suggéré.

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