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LOCAL CONTROL OF CIRCULATION

ANG II-induced downregulation of RBF after a prolonged reduction of renal perfusion pressure is due to pre- and postglomerular constriction

¹Department of Medical Physiology, Division of Renal and Cardiovascular Research, The Panum Institute, University of Copenhagen, DK-2200 Copenhagen N; and ²Department of Physiology and Pharmacology, The University of Southern Denmark, DK-5000 Odense C, Denmark

Submitted 29 July 2003 ; accepted in final form 7 January 2004

Previous experiments from our laboratory showed that longer-lasting reductions in renal perfusion pressure (RPP) are associated with a gradual decrease in renal blood flow (RBF) that can be abolished by clamping plasma ANG II concentration ([ANG II]). The aim of the present study was to investigate the mechanisms behind the RBF downregulation in halothane-anesthetized Sprague-Dawley rats during a 30-min reduction in RPP to 88 mmHg. During the 30 min of reduced RPP we also measured glomerular filtration rate (GFR), proximal tubular pressure (P_prox), and proximal tubular flow rate (Q_LP). Early distal tubular fluid conductivity was measured as an estimate of early distal [NaCl] ([NaCl]_ED), and changes in plasma renin concentration (PRC) over time were measured. During 30 min of reduced RPP, RBF decreased gradually from 6.5 ± 0.3 to 6.0 ± 0.3 ml/min after 5 min (NS) to 5.2 ± 0.2 ml/min after 30 min (P < 0.05). This decrease occurred in parallel with a gradual increase in PRC from 38.2 ± 11.0 x 10^-5 to 87.1 ± 25.1 x 10^-5 Goldblatt units (GU)/ml after 5 min (P < 0.05) to 158.5 ± 42.9 x 10^-5 GU/ml after 30 min (P < 0.01). GFR, P_prox, and [NaCl]_ED all decreased significantly after 5 min and remained low. Estimates of pre- and postglomerular resistances showed that the autoregulatory mechanisms initially dilated preglomerular vessels to maintain RBF and GFR. However, after 30 min of reduced RPP, both pre- and postglomerular resistance had increased. We conclude that the decrease in RBF over time is caused by increases in both pre- and postglomerular resistance due to rising plasma renin and ANG II concentrations.

renal vascular resistance; autoregulation; glomerular filtration rate

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