Nephrology Dialysis Transplantation, Vol 13, Issue 12 3065-3073, Copyright © 1998 by Oxford University Press
A Nilsson, M Adams, S Matthews, G Guron, B Sundelin and P Friberg
Background. Neonatal inhibition of the
renin-angiotensin system (RAS) causes a decreased urinary concentrating
ability, papillary atrophy, and tubulointerstitial inflammation long term.
As a consequence of these morphological changes, we surmised that renal
blood flow and renal interstitial hydrostatic pressure (RIHP) may be
altered during and shortly after cessation of neonatal
angiotensin-converting enzyme (ACE) inhibition, and that tentative changes
of these variables would persist long after treatment withdrawal.
Methods. Rats were given daily intraperitoneal
injections of the ACE inhibitor, enalapril (10 mg/kg) or saline from days 3
to 23 postpartum, and the relationship between renal perfusion pressure
(PP) and RIHP was investigated in 6- and 13-week-old anaesthetized rats.
Results. Neonatal ACE inhibition did not affect
baseline RIHP short term, whereas RIHP was reduced at 13 weeks of age
versus controls (11.6±1.6 vs
18.5±1.0 mmHg, P<0.05). Changes in
RIHP correlated positively to changes in renal PP, independent of treatment
and age (slope averaged 0.11±0.03). Ongoing ACE inhibition until
6 weeks of age neither affected baseline RIHP nor altered the reactivity to
changes in perfusion pressure. Mild renal histopathological abnormalities
were present already 3 weeks after cessation of treatment and were
aggravated significantly in the 13-week-old rats, showing a complete loss
of the papillary parenchyma. Conclusion. The reduced
baseline RIHP in adult rats seemed to constitute a functional correlate to
the major papillary atrophy. However, RIHP responses to changes in renal
perfusion pressure was maintained, possibly indicating a compensatory
effect of the remaining vasa recta and/or peritubular capillary network.
Taken together, lack of neonatal angiotensin II type-1 (AT1) receptor
stimulation induces not only irreversible abnormalities of the renal
architecture, but causes alteration of intrarenal haemodynamics, such as a
reduced RIHP, which may have implications for the regulation of
pressure-natriuresis. Keywords: neonate; rat; renal
blood flow; renal interstitial hydrostatic pressure; renal perfusion
pressure; renin-angiotensin system
ORIGINAL ARTICLES
Long-term reduction of renal interstitial hydrostatic pressure after neonatal renin-angiotensin system inhibition in the rat
Department of Physiology, Institute of Physiology and Pharmacology, Goteborg University, Medicinaregatan 11, S-413 90 Goteborg, Sweden; Department of Pharmacology and Toxicology, Queens University, Ontario, Canada; Department of Pathology, Karolinska Hospital, Stockholm, Sweden; Clinical Physiology, Sahlgrenska University Hospital, Sweden; Corresponding author
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