Kinin and tubuloglomerular feedback in normal and hydronephrotic rats.
The role of bradykinin in resetting the tubuloglomerular feedback (TGF) mechanism was studied with the stop-flow technique in control and hydronephrotic Inactin-anesthetized rats. Glomerular function was assessed by measuring stop-flow pressure (Psf); the maximal decrease in stop-flow pressure (delta Psf) with increased loop of Henle perfusion and the perfusion that elicited half-maximal delta Psf, the turning point (TP), were determined. Bradykinin infusion resulted in resetting of TGF in both control and hydronephrotic rats but in different directions. A decreased sensitivity was found in control rats (TP increased from 18.6 to 26.4 and 16.8 to 22.1 nl/min on systemic and intratubular administration, respectively). In hydronephrotic rats the sensitivity of TGF increased. TP decreased from 19.9 to 15.2 nl/min with bradykinin administered systemically and from 18.4 to 15.0 nl/min on intratubular administration. These results show that exogenous kinin administration mimics the effects of extracellular volume expansion on TGF resetting and demonstrate a difference in resetting in hydronephrotic and control kidneys.
Morsing
P
P
Department of Physiology and Biophysics, University of Lund, Sweden.
Persson
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D000818:Animals; D001920:Bradykinin / Q000008:administration & dosage / Q000494:pharmacology*; D005246:Feedback / Q000502:physiology; D006869:Hydronephrosis / Q000503:physiopathology*; D007261:Infusions, Intra-Arterial; D007678:Kidney Glomerulus / Q000187:drug effects* / Q000502:physiology; D007684:Kidney Tubules / Q000187:drug effects* / Q000502:physiology; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains
D001920:Bradykinin