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Am J Physiol Heart Circ Physiol (February 14, 2002). doi:10.1152/ajpheart.01124.2001
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Articles in PresS, published online ahead of print February 14, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.01124.2001
Submitted on December 27, 2001
Accepted on February 13, 2002

Impaired Endothelium-Mediated Relaxation in Isolated Cerebral Arteries from 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.

Insulin resistance (IR) impairs vascular responses in peripheral arteries. However, the effects of IR on cerebrovascular control mechanisms are completely unexplored. We examined the vascular function of isolated middle cerebral arteries (MCA) from fructose-fed IR and control rats. Endothelium-dependent vasodilation, elicited by bradykinin (BK) was reduced in IR compared to control MCAs. Maximal dilation to BK (10-6 M) was 38±3 % (n=13) in control and 19±3 % (n=10) in IR arteries (p<0.01). L-NAME (10µM) decreased responses to BK in control arteries by ~65 % and inhibited the already reduced responses completely in IR MCAs. Indomethacin (10µM) reduced relaxation to BK in control MCAs by ~40 %, but was largely ineffective in the IR arteries. Combined L-NAME and indomethacin treatments eliminated the BK-induced dilatation in both groups. Similarly to BK, endothelium-mediated and mainly cyclooxygenase (COX) dependent dilation to calcium ionophore A23187 was reduced in IR arteries compared to controls. In contrast, vascular relaxation to sodium nitroprusside was similar between the IR and control groups. These findings demonstrate that endothelium-dependent dilation in cerebral arteries is impaired in IR primarily due to a defect of the COX-mediated pathways. In contrast, nitric-oxide-mediated dilation remains intact in IR arteries.




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