期刊
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
卷 282, 期 6, 页码 H2060-H2065出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpheart.01124.2001
关键词
middle cerebral artery; bradykinin; A23187; nitric oxide; cyclooxygenase
资金
- NHLBI NIH HHS [HL-50587, HL-46558, HL-30260, HL-66074] Funding Source: Medline
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 (MCAs) from fructose-fed IR and control rats. Endothelium-dependent vasodilation elicited by bradykinin (BK) was reduced in IR compared with 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). N-ω-nitro-L-arginine methyl ester (L-NAME; 10 μM) decreased responses to BK in control arteries by ∼65% and inhibited the already reduced responses completely in IR MCAs. Indomethacin (10 μM) reduced relaxation to BK in control MCAs by ∼40% but was largely ineffective in IR arteries. Combined L-NAME and indomethacin treatments eliminated the BK-induced dilation in both groups. Similarly to BK, endothelium-mediated and mainly cyclooxygenase (COX)-dependent dilation to calcium ionophore A23187 was reduced in IR arteries compared with 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 because of a defect of the COX-mediated pathways. In contrast, nitric oxide-mediated dilation remains intact in IR arteries.
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