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II PKC activation
Department of Physiology and Biophysics, Indiana University Medical School, Indianapolis, Indiana 46202
II protein
kinase C (PKC) is activated during acute and chronic hyperglycemia
and may alter endothelial cell function. We determined whether blockade
of PKC protected in vivo endothelial formation of NO, as measured
with NO-sensitive microelectrodes in the rat intestinal vasculature.
NaCl hyperosmolarity, a specific endothelial stimulus to increase NO
formation, caused ~20% arteriolar vasodilation and ~30% increase
in NO concentration ([NO]). After topical 300 mg/dl hyperglycemia for
45 min, both responses were all but abolished. In comparison,
pretreatment with LY-333531, a specific PKC inhibitor, maintained
vasodilation and [NO] responses to NaCl hyperosmolarity after
hyperglycemia. The PKC inhibitor alone had no significant effects on
resting diameter or [NO] or their responses to NaCl hyperosmolarity.
In separate rats, after topical hyperglycemia had suppressed dilation
to ACh, LY-333531 restored ~70% of the dilatory response. These data
demonstrated that activation of PKC during acute hyperglycemia
depressed in vivo endothelial formation of NO at rest and during
stimulation. This abnormality can be minimized by inhibition of PKC
before hyperglycemia and can be substantially reversed by PKC
inhibition after hyperglycemia-induced abnormalities have occurred.
protein kinase C; arteriole
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