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1-adrenoceptor antagonist on diabetes-induced changes in peripheral nerve function, metabolism, and antioxidative defense
Division of Endocrinology and Metabolism, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, Michigan 48109-0354, USA
1Correspondence: Division of Endocrinology and Metabolism, Department of Internal Medicine, University of Michigan Medical Center, 1150 West Medical Center Dr., MSRB II, Rm. 5570, Ann Arbor, MI 48109-0354, USA. E-mail: iobrosso{at}umich.edu
The role for nerve blood flow (NBF) vs. other factors in motor
nerve conduction (MNC) slowing in short-term diabetes was assessed by
evaluating 
1-adrenoceptor antagonist prazosin on NBF,
MNC, as well as metabolic imbalances and oxidative stress in the neural
tissue. Control and diabetic rats were treated with or without prazosin
(5 mg·kg-1·d-1 for 3 wk). NBF was
measured by hydrogen clearance. Both endoneurial vascular
conductance and MNC velocity were decreased in diabetic rats vs.
controls, and this decrease was prevented by prazosin. Free
NAD+:NADH ratios in mitochondrial cristae, matrix, and
cytosol assessed by metabolite indicator method, as well as
phosphocreatine levels and phosphocreatine/creatine ratios, were
decreased in diabetic rats, and this reduction was ameliorated by
prazosin. Neither diabetes-induced accumulation of two major glycation
agents, glucose and fructose, as well as sorbitol and total
malondialdehyde plus 4-hydroxyalkenals nor depletion of
myo-inositol, GSH, and taurine or decrease in
(Na/K)-ATP-ase activity were affected by prazosin. In conclusion,
decreased NBF, but not metabolic imbalances or oxidative stress in the
neural tissue, is a key mechanism of MNC slowing in short-term
diabetes. Further experiments are needed to estimate whether
preservation of NBF is sufficient for prevention of nerve dysfunction
and morphological abnormalities in long-standing diabetes or whether
the aforementioned metabolic imbalances closely associated with
impaired neurotropism are of greater importance in advanced than in
early diabetic neuropathy.—Obrosova, I. G., Van Huysen, C.,
Fathallah, L., Cao, X., Stevens, M. J., Greene, D. A.
Evaluation of 1-adrenoceptor antagonist on
diabetes-induced changes in peripheral nerve function, metabolism, and
antioxidative defense.
Key Words: motor nerve conduction • peripheral diabetic neuropathy • nerve blood flow • prazosin
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