<p>This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</p> <p>
            <italic>Aim</italic> The effect of 8 weeks′ streptozotocin (STZ)-
induced diabetes and aminoguanidine (AMNG), the
inhibitor of advanced glycosylation reaction, treatment
on arteriolar reactivity to vasoactive substances
was investigated <italic>in vitro</italic>.</p> <p>
            <italic>Materials and Methods</italic> Studies were performed in
untreated control rats (<italic>n</italic> = 10), STZ-induced (60 mg/kg
i.v.) diabetic rats (<italic>n</italic> = 10), AMNG-treated (600 mg/l
given in drinking water throughout 8 weeks) control
rats (<italic>n</italic> = 10) and AMNG-treated (600 mg/l given in
drinking water, beginning at 72h after STZ and
throughout 8 weeks of diabetes) diabetic rats (<italic>n</italic> = 10).
Results are expressed as the mean ±s.e. Relaxant
responses are expressed as a percentage (%) relaxation
of noradrenaline-induced tone. Statistical comparisons
were made by one-way analysis of variance
(ANOVA) followed by Tukey–Kramer multiple
comparisons test.</p> <p>
            <italic>Results</italic> 1. The decreased body weights (205 ± 6 g)
and increased blood glucose levels (583 ± 8 mg/dl) of
diabetic rats were partially restored by treatment of
aminoguanidine (253 ± 6 g, <italic>p</italic> &lt; 0.05 and 480 ± 14 mg/dl, <italic>p</italic> &lt; 0.001, respectively). 2. Diabetes caused a 71%
deficit in maximal endothelium-dependent relaxation
to acetylcholine for noradrenaline precontracted
aortas (<italic>p</italic> &lt; 0.001). AMNG treatment prevented the
diabetes-induced impairment in endothelium dependent
relaxation (58 ± 8%) to acetylcholine, maximum
relaxation remaining in the non-diabetic range
(78 ± 4%). 3. Neither diabetes nor treatment affected endothelium-independent relaxation (pD<sub>2</sub> and max.
Relax.) to sodium nitroprusside. 4. Vasoconstrictor
responses (pD<sub>2</sub> and Max. Contraction) to noradrenaline
and KCl were not influenced by the diabetic
state and treatment.</p> <p>
            <italic>Conclusion</italic> Our data suggest that 8 weeks of
experimental diabetes is associated with a decreased
endothelium-dependent vasodilatation. AMNG
treatment may prevent diabetes-induced endothelial
dysfunction. This may be mediated <italic>via</italic> the prevention
of advanced glycosylation end product formation,
the enhanced release of vasodilator substances
such as prostacyclin, the increased elasticity of blood
vessels, the antioxidant activity and inhibitor activity
of enzyme aldose-reductase by AMNG.</p>
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Int J Exp Diabetes Res. 2000; 1(2):145-153