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Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi 39216
Nitric oxide (NO) plays an important role in the
regulation of vascular tone, and evidence suggests that
endothelial-dependent relaxation, possibly mediated via NO, is impaired
in diabetes. However, the role of the endothelium in arterial pressure
control early in diabetes, before dysfunction develops, is not known. This was evaluated in the present study by comparing the responses to
induction of diabetes in vehicle-treated rats (D, n = 7) vs. rats chronically treated with
NG-nitro-L-arginine methyl ester
(L-NAME; D+L, n = 8). A nondiabetic group
also was treated with L-NAME (L, n = 7) to
control for L-NAME effects over time, independent of
diabetes. After baseline measurements, rats were given either vehicle
or L-NAME (10 µg · kg
1 · min1 iv)
infusion throughout the experiment. Six days later, streptozotocin (60 mg/kg iv) was administered, followed by a 3-wk diabetic study period.
Induction of diabetes in the D+L rats caused a marked and progressive
increase in mean arterial pressure throughout the diabetic period,
averaging ~70 mmHg greater than in the D rats and ~20 mmHg greater
than in the L rats. Glomerular filtration rate and renal plasma flow
tended to increase during diabetes, but this trend was reversed in the
D+L rats. In addition, plasma renin activity increased in the D and D+L
rats during week 1 of diabetes but then returned to control
in the D rats, while continuing to increase in the D+L rats. These
results suggest that, in the early stages of diabetes, NO synthesis is
important to prevent hypertension from developing, possibly through
actions to maintain glomerular filtration and suppress renin secretion.
NG-nitro-L-arginine methyl ester; arterial pressure; glucose; angiotensin II; vasodilation
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