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Am J Physiol Heart Circ Physiol (August 8, 2002). doi:10.1152/ajpheart.00516.2002
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Articles in PresS, published online ahead of print August 8, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00516.2002
Submitted on June 21, 2002
Accepted on July 26, 2002

Alterations in Calcium-Activated and ATP-Dependent Potassium Channel Function in Cerebral Arteries of Insulin Resistant Rats

Benedek Erdos1*, Allison W Miller2, and David W Busija2

1 Department of Physiology and Pharmacology, Wake Forest University School of Medicine, Winston-Salem, NC, USA; Institute of Human Physiology and Clinical Experimental Research, Semmelweis University, Budapest, Hungary
2 Department of Physiology and Pharmacology, Wake Forest University School of Medicine, Winston-Salem, NC, USA

* To whom correspondence should be addressed. E-mail: berdos{at}wfubmc.edu.

In the present study, we examined whether insulin resistance (IR) alters the function of ATP-dependent and calcium-activated potassium channels (K+ATP- and K+Ca-channels) in pressurized isolated middle cerebral arteries (MCA) from fructose-fed IR and control rats. Blockade of the K+Ca-channels with tetra-ethyl-ammonium-chloride (TEA, 2.5 mM) or iberiotoxin (IBTX, 0.1µM) increased the spontaneously developed tone in the control MCAs by 10.5±1.3% (n=10) and 13.3±2.3% (n=6), respectively. In the IR arteries, TEA induced similar constrictions (8.0±1.1%, n=10), but IBTX constricted the IR arteries only by 3.1±0.9% (n=8, p<0.01). Bradykinin (BK)-induced endothelium-mediated relaxation was reduced in IR MCAs. Maximum relaxation to BK (10-6 M) was 42±4% in control (n=9) and 19±2% in IR arteries (n=10, p<0.01). Pretreatment with TEA, IBTX or the K+ATP-channel blocker glibenclamide (10µM) inhibited the relaxation to BK in control MCAs, but did not alter dilation in IR arteries. Relaxation to the channel-opener cromakalim (CR) was also diminished in the IR MCAs. Maximum relaxation to CR (10-5 M) was 48±3% in control (n=6) and 19±2% in IR arteries (n=6, p<0.01). These findings demonstrate that IR alters the function of the K+ATP- and K+Ca-channels in isolated MCAs and affects the control of resting vascular tone and the mediation of dilator stimuli.




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