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Am J Physiol Heart Circ Physiol 280: H621-H627, 2001;
0363-6135/01 $5.00
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Vol. 280, Issue 2, H621-H627, February 2001

Arteriolar nitric oxide concentration is decreased during hyperglycemia-induced beta II PKC activation

H. Glenn Bohlen and Geoffrey P. Nase

Department of Physiology and Biophysics, Indiana University Medical School, Indianapolis, Indiana 46202

beta II protein kinase C (beta PKC) is activated during acute and chronic hyperglycemia and may alter endothelial cell function. We determined whether blockade of beta 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 beta PKC inhibitor, maintained vasodilation and [NO] responses to NaCl hyperosmolarity after hyperglycemia. The beta 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 beta PKC during acute hyperglycemia depressed in vivo endothelial formation of NO at rest and during stimulation. This abnormality can be minimized by inhibition of beta 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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