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Vascular Biology Center, Department of Surgery and Department of Physiology and Endocrinology, Medical College of Georgia, Augusta, Georgia 30912-2500
Experiments were conducted to determine
whether Sprague-Dawley rats from different suppliers have the same
hypertensive response to chronic inhibition of nitric oxide synthase.
Rats (240-260 g) obtained from either Harlan or Charles River
Laboratories were maintained in metabolic cages for baseline
(week
0) measurements before receiving
N
-nitro-L-arginine methyl ester
(L-NAME) in the
drinking water for 2 wk at 5 or 65 mg · kg
1 · day
1.
Baseline values for tail cuff pressure (TCP) were significantly higher
in Harlan rats (131 ± 2 mmHg) compared with Charles River rats
(108 ± 3 mmHg, P < 0.001). At 65 mg · kg
1 · day
1,
L-NAME produced a significantly
larger increase in TCP in Harlan versus Charles River rats (41 ± 4 vs. 29 ± 4%, respectively,
P < 0.01). Food and water
intake and sodium and water excretion were not different between
groups. Urinary excretion of nitrate and nitrite
(UNOxV) was
significantly reduced in all rats given L-NAME.
UNOxV was
decreased by 69 ± 12 and 62 ± 7% in Harlan and Charles River
rats, respectively. The lower dose of
L-NAME increased TCP and
decreased UNOxV
in both Harlan and Charles River rats; these effects were more
pronounced in the Harlan rats. These results suggest that NO plays a
more significant role in the maintenance of arterial pressure in
Sprague-Dawley rats from Harlan compared with Charles River
Laboratories. Such findings may also provide insight as to why some of
the mechanisms associated with chronic L-NAME treatment are not
consistent between laboratories.
N
-nitro-L-arginine methyl
ester; urinary nitrate and nitrite
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