EVIDENCE FOR ACUTE RENAL CORTICAL VASOCONSTRICTION AFTER UNINEPHRECTOMY

Citation
Dw. Moskowitz et al., EVIDENCE FOR ACUTE RENAL CORTICAL VASOCONSTRICTION AFTER UNINEPHRECTOMY, Renal failure, 18(6), 1996, pp. 833-846
Citations number
48
Categorie Soggetti
Urology & Nephrology
Journal title
ISSN journal
0886022X
Volume
18
Issue
6
Year of publication
1996
Pages
833 - 846
Database
ISI
SICI code
0886-022X(1996)18:6<833:EFARCV>2.0.ZU;2-Y
Abstract
The rate of progression of chronic renal failure (CRF) is similar for many diseases, suggesting a common, perhaps intrinsic, renal signal fo r its progression. The remnant nephron hypothesis of Bricker suggests that CRF may be the result of persistent compensatory renal growth (CR G). Normally, CRG after unilateral nephrectomy (uniNx) ceases within 1 week. Knowledge of the signals that initiate CRG may therefore shed l ight on the signals responsible for ongoing CRF. The signals responsib le for the initiation of compensatory renal growth after uniNx are unk nown. Hemodynamic changes in the remaining renal artery have been obse rved, but there are as yet no data for the main renal compartment whic h undergoes hypertrophy, the superficial renal cortex. The noninvasive technique of laser-Doppler flowmetry allows the continuous and indepe ndent monitoring of blood velocity and blood volume. The product of th e two signals is proportional to tissue blood flow per unit volume of the tissue observed. Under controlled conditions in adult male Sprague -Dawley rats, renal cortical blood velocity increased by 22% within 5 min after uniNx and remained elevated at this level for 60 min. Renal cortical blood volume decreased throughout the experiment. Their produ ct, renal cortical blood flow, increased briefly by 14% 5 min after un iNx but decreased over the time of observation in parallel with renal cortical blood volume. The simultaneous increase in blood velocity and decrease in blood volume in the superficial renal cortex acutely afte r uniNx suggest that vasoconstriction is an early event in compensator y renal growth.