Nephrology Dialysis Transplantation, Vol 13, Issue 4 893-899, Copyright © 1998 by Oxford University Press
G Verseput, B Braam, A Provoost and H Koomans
Background: The spontaneously hypertensive fawn-hooded
(FHH) rat develops severe glomerulosclerosis with ageing. The afferent
arteriolar resistance is low, resulting in a strongly elevated glomerular
capillary pressure (PGC). Methods: Afferent arteriolar
resistance is under the control of the tubuloglomerular feedback (TGF)
system, and we studied whether young FHH rats, i.e. at a stage when only
mild glomerulosclerosis was present, have diminished TGF responsiveness.
Results: Maximum TGF-mediated decreases in stop-flow
pressure in response to late proximal perfusion with artificial tubular
fluid were 9.0±1.0 mmHg, a value not different or even slightly
lower than observed in normal rats. PGC was 59.9±1.2 mmHg and
the estimated PGC was 59.9±1.2 mmHg and the estimated PGC at
half-maximal activation of the TGF system (operating PGC) was
54.5±0.8 mmHg at 11 weeks of age (n=11), a value higher than
observed in normal rats. The second question of the present study concerns
the effect of chronic angiotensin-I-converting enzyme inhibitor (ACE-I)
administration on PGC-ACE-I, by reducing angiotensin II (Ang II)
availability, diminishes TGF responsiveness, which would offset the
beneficial effect on PGC under normal flow conditions to the macula densa.
Maximum TGF responses were 8.9±1.0 and 17.5±1.5 mm Hg
in 11- and 26-week-old rats that had been treated with the ACE-I lisinopril
in the drinking water started when the animals were 7 weeks of age. PGC was
44.3±1.2 (n=9) and operating PGC was 40.1±1.6 mmHg
(n=9) at 11, values significantly lower than in untreated rats. Values
remained lower in the 26-week-old treated animals and were
40.9±0.8 and 32.6±1.1 mm Hg.
Conclusions: 91) the TGF system in this model of
spontaneous hypertension and glomerulosclerosis is intact, despite the fact
that the FHH rat has a characteristically low afferent arteriolar
resistance as compared to other hypertensive rats; (2) the rat displays a
normal or even enhanced function of the TGF system following prolonged
administration of the ACE-I lisinopril. The latter finding indicates that
the reduction of PGC achieved by the ACE-I is not offset by a concomitant
attenuation of TGF function.
ORIGINAL ARTICLES
Tubuloglomerular feedback and prolonged ACE-inhibitor treatment in the hypertensive fawn-hooded rat
Department of Nephrology and Hypertension, Room F03. 226, University Hospital Utrecht, PO Box 85500, 3508 GA Utrecht, The Netherlands; Department of Pediatric Surgery, Erasmus University, Rotterdam, The Netherlands; Corresponding author
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