Hypertension, Vol 23, 752-756, Copyright © 1994 by American Heart Association
H Hayakawa, Y Hirata, E Suzuki, K Kimura, K Kikuchi, T Nagano, M Hirobe and M Omata
To examine the effects of L-arginine (L-Arg) on endothelial function, we
administered 0.5 g/L L-Arg in drinking water to deoxycorticosterone acetate
(DOCA)-salt rats for 8 weeks and then measured nitric oxide (NO) release
from isolated kidneys using a newly developed real-time chemiluminescence
method. Renal pathology was also analyzed. Acetylcholine caused much
smaller declines in renal perfusion pressure (10(-7) mol/L acetylcholine:
-24 +/- 2% [SEM] versus -50 +/- 2%, P < .001) and NO release in
DOCA-salt rats (+3 +/- 1 versus +33 +/- 3 fmol/min per gram kidney weight,
P < .001) compared with control rats. L-Arg did not influence the time
course of systolic blood pressure elevation in DOCA-salt rats (211 +/- 5
versus 208 +/- 6 mmHg, DOCA versus L-Arg/DOCA, P = NS). However, oral
administration of L-Arg improved acetylcholine-induced declines in renal
perfusion pressure (10(-7) mol/L acetylcholine: L-Arg/DOCA, -39 +/- 3%, P
< .01 versus DOCA). This change was associated with an increase in NO
release by acetylcholine (10(-7) mol/L acetylcholine: L-Arg/DOCA, +10 +/- 1
fmol/min per gram kidney weight, P < .05 versus DOCA). However,
morphological changes in renal vessels and glomeruli were similar between
DOCA and L-Arg/DOCA rats. These results suggest that L-Arg administration
partially reverses renal endothelial function with respect to
vasorelaxation and NO release independent of blood pressure changes,
indicating that hypertensive vessels seem to be depleted of L- Arg and/or
have defects in the availability of L-Arg for NO synthesis.
ARTICLES
Long-term administration of L-arginine improves nitric oxide release from kidney in deoxycorticosterone acetate-salt hypertensive rats
Second Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.
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