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Department of Physiology, New York Medical College, Valhalla, New York 10595
In this study we
tested the hypothesis that C-peptide alone or in conjunction with
insulin may cause a dilation of skeletal muscle arterioles. First-order
arterioles (88 µm) isolated from rat cremaster muscles were
pressurized (65 mmHg), equilibrated in a Krebs bicarbonate-buffered
solution (pH 7.4), gassed with 10%
O2 (balance 5%
CO2, 85%
N2), and studied in a no-flow
state. C-peptide administered at concentrations of 0.3, 1, 3, 10, 100, 300, and 1,000 ng/ml evoked arteriolar dilation that was not
concentration dependent. In contrast, the administration of the four
lower physiological concentrations of C-peptide to arterioles exposed
to a nondilating concentration of insulin evoked a significant
concentration-dependent increase in arteriolar diameter from 8.6 to
42.3% above control. The arteriolar dilation to C-peptide in the
presence of insulin was completely inhibited by administration of
NG-nitro-L-arginine
(10
4 M). Responses to ACh
and adenosine were not enhanced when these drugs were administered in
the presence of insulin. These results indicate that C-peptide has the
capacity to evoke arteriolar dilation in skeletal muscle via a nitric
oxide-mediated mechanism that appears to be enhanced by an interaction
with insulin. Furthermore, the effects of insulin appear to be specific
for C-peptide and are not the result of a general enhancement of
endothelium-dependent or endothelium-independent dilation.
microcirculation; vasodilation; rats; insulin-dependent diabetes mellitus; arterioles; nitric oxide; NG-nitro-L-arginine; vascular smooth muscle; endothelium
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