AJP - Renal Physiology, Vol 258, Issue 4 1026-F1035, Copyright © 1990 by American Physiological Society
Acute and subacute prostaglandin and ANG II inhibition on glomerulotubular dynamics in rats
B. J. Tucker and R. C. Blantz
Department of Medicine, University of California, San Diego School of Medicine, La Jolla 92093.
Prostaglandins (PG) and angiotensin II (ANG II) contribute to regulation of
glomerular microcirculation. Acute vs. chronic physiological alterations of
glomerular hemodynamics that result from inhibition of either PG or ANG II,
or both, and their interaction were examined. Four groups of Munich-Wistar
rats were submitted to the following micropuncture studies in euvolemic
conditions for measurements of glomerular hemodynamics and tubular fluid
reabsorption: 1) an untreated control group, 2) 4- to 6-day inhibition of
both PG and angiotensin-converting enzyme activity with meclofenamate and
MK-421 (enalapril), 3) 4- to 6-day treatment with enalapril followed by
acute PG inhibition in the second measurement period, 4) 4- to 6-day PG
inhibition followed by acute enalapril treatment in the second period. Dual
4- to 6-day treatment decreased single-nephron filtration rate (SNGFR, 24
+/- 2 vs. 33 +/- 2 nl/min in control; P less than 0.05) as a result of
decreases in single-nephron plasma flow (SNPF) and glomerular hydrostatic
pressure gradient (delta P). Treatment with enalapril alone for 4-6 days
did not reduce SNGFR and SNPF; however, delta P decreased. Acute addition
of meclofenamate did not alter these factors. SNGFR was decreased with 4-
to 6-day treatment of meclofenamate from 33 +/- 2 in control to 25 +/- 1
nl/min (P less than 0.05). Acute treatment with enalapril in the 4- to
6-day meclofenamate-treated rats increased SNGFR to values not different
from control. The results demonstrated that glomerular hemodynamic
alterations consequent to inhibition of ANG II and PG systems differ
between chronic and acute treatments. Therefore, interpretation of the role
of individual hormonal systems in the control of glomerular hemodynamics
should be approached with caution, since effects may be altered by duration
of treatment and involvement of other vasoactive systems.
