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1 Section of Nephrology, Department of Medicine, and 2 Department of Urology, Case Western Reserve University, Department of Veterans Affairs Medical Center, Cleveland, Ohio 44106
Changes in
activity or expression of protein kinase C (PKC), reactive oxygen
products, and nitric oxide (NO) may account for the alteration in cell
behavior seen in diabetes. These changes have been proposed to be part
of the pathophysiology of erectile dysfunction. We sought to ascertain
if corpus cavernosal vascular smooth muscle cells (CCSMC) grown in a
high glucose milieu exhibit changes in the activity and expression of
PKC isoforms, NO, and reactive oxygen products and to find out if these
changes are prevented by 
-tocopherol. Rat CCSMC were
grown in 5, 15, and 30 mM glucose concentrations for 3, 7, and 14 days.
PKC isoform expression was assayed with isoform-specific antibodies. In
CCSMCs grown in 30 mM glucose for 2-wk, PKC-
2-isoform
was upregulated (n = 4; P < 0.01), whereas the
expression of -, 
-, 
-, and 1-isoforms was
unchanged. NO as measured by nitrate-to-nitrite ratio was greatly
diminished at 14 days in 30 mM (n = 4; P < 0.002)
compared with 5 mM glucose. Reactive oxygen products were upregulated
at 14 days when they were assayed by the fluorescent probe
dichlorofluorescein diacetate bis(acetoxy-methyl) (DCFH-DA) (n = 5; P < 0.01). When these same cells were
exposed to -tocopherol for 14 days, there was a reduction of
PKC-2 (57.8%; P < 0.01; n = 4) and a reduction in reactive oxygen product formation (71.1%;
P < 0.001; n = 4), along with an increase in
nitrate-to-nitrite ratio (43.9%; P < 0.01, n = 4). These results suggest that there may be an
interrelationship between PKC, NO, and reactive oxygen product
formation in CCSMC exposed to a high glucose environment.
diabetes mellitus; nitric oxide synthase; protein kinase
C-2
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