Hypertension, Vol 21, 956-960, Copyright © 1993 by American Heart Association
T Nakamura, AM Alberola and JP Granger
The role of renal interstitial pressure was examined in mediating the
sodium retention induced by blockade of nitric oxide synthesis. The effects
of intravenous NG-nitro-L-arginine-methyl ester (L-NAME), a synthesis
inhibitor, on renal hemodynamics, renal interstitial hydrostatic pressure,
and sodium and lithium excretion were determined. L-NAME (50 micrograms/kg
per minute) was infused for 75 minutes in Sprague-Dawley rats (n = 7) in
which renal perfusion pressure was permitted to rise in parallel with
systemic arterial pressure and in rats (n = 8) in which renal perfusion
pressure was serocontrolled constant at basal levels. Infusion of L-NAME
raised renal perfusion pressure from 122 +/- 6 to 157 +/- 4 mm Hg in the
nonservocontrolled group but not in the servocontrolled group (118 +/- 3 mm
Hg). L-NAME decreased renal plasma flow and glomerular filtration rate to
the same level in both rat groups. L-NAME significantly decreased sodium
excretion (1.38 +/- 0.41 to 0.36 +/- 0.14 microEq/min and 1.19 +/- 0.46 to
0.30 +/- 0.05 microEq/min, respectively), fractional excretion of lithium
(25.7 +/- 1.7% to 16.7 +/- 2.3% and 25.6 +/- 4.0% to 18.2 +/- 1.7%), and
renal interstitial hydrostatic pressure (6.4 +/- 1.4 to 3.2 +/- 0.9 mm Hg
and 6.3 +/- 1.8 to 2.7 +/- 0.9 mm Hg) in servocontrolled and
nonservocontrolled groups. However, there was no significant difference in
the renal hemodynamic and excretory responses to L-NAME between the
servocontrolled and nonservocontrolled groups. In summary, reductions in
sodium excretion during inhibition of nitric oxide synthesis are associated
with significant reductions in renal interstitial hydrostatic
pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
ARTICLES
Role of renal interstitial pressure as a mediator of sodium retention during systemic blockade of nitric oxide
Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson 39216-4505.
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