Resetting of exaggerated tubuloglomerular feedback activity in
acutely volume expanded young spontaneously hypertensive rats.
Br[umlaut]annstr[diaeresis]om, Kristina, and William J. Arendshorst.
Department of Cell and Molecular Physiology, University of North
Carolina at Chapel Hill, Chapel Hill, N.C.
APStracts 5:0188F, 1998.
One purpose of the present study was to evaluate the ability of 7-wk
-old spontaneously hypertensive rats (SHR) to reset tubuloglomerular
feedback (TGF) activity in response to acute volume expansion (VE).
Secondly, we evaluated the contribution of angiotensin II via its
action on AT1 receptors to TGF control of glomerular function during
VE. TGF was assessed by micropuncture methods and proximal tubular
stop-flow pressure (SFP) determinations in SHR, Wistar-Kyoto rats
(WKY) and Sprague-Dawley rats (SD). During euvolemia SHR exhibited
enhanced TGF activity. In the same animals acute VE was achieved by
infusion of saline
(5 ml/hr/100g BW). VE led to resetting of TGF in all three strains.
Maximal SFP responses, elicited by a 30-40 nl/min loop of Henle
perfusion rate, decreased from 19 to 12 mmHg in SHR, and on average
from 11 to 5 mmHg in WKY and SD (P<0.001). Tubular flow rate
producing a half-maximal response (turning point) shifted to higher
flow rates during VE, from 12 to 14 nl/min in SHR and from 15 to 19
nl/min in WKY. Administration of the AT1 receptor blocker candesartan
(0.05 mg/kg iv) during sustained VE decreased TGF-mediated reductions
in SFP in SHR and slightly increased the turning point in WKY.
Nevertheless, other parameters of TGF activity were unaffected by AT1
receptor blockade. In conclusion, young SHR possess the ability to
reset TGF activity in response to VE to a degree similar to
compensatory adjustments in WKY. However, TGF remains enhanced in SHR
during VE. Angiotensin II and its action on AT1 receptors is in part
responsible for the exaggerated SFP responses in young SHR during VE.
Received 10 August 1998; accepted in final form 15 October 1998
APS Manuscript Number F201-8.
Article publication pending Am. J. Physiol. (Renal Physiology).
ISSN 1080-4757 Copyright 1998 The American Physiological Society.
Published in APStracts on 10 November 1998