COX-2 contributes to the maintenance of flow-induced dilation in arterioles of eNOS-knockout mice.

American Journal of Physiology. Heart and Circulatory Physiology
Dong SunGabor Kaley

Abstract

Our previous studies demonstrated that, in gracilis muscle arterioles of male mice deficient in the gene for endothelial nitric oxide synthase (eNOS), flow-induced dilation (FID) is mediated by endothelial PGs. Thus the present study aimed to identify the specific isoform of cyclooxygenase (COX) responsible for the compensatory mediation of FID in arterioles of eNOS-knockout (KO) mice. Experiments were conducted on gracilis muscle arterioles of male eNOS-KO and wild-type (WT) mice. Basal tone and magnitude of FID of arterioles were comparable in the two strains of mice. A role for COX isoforms in the mediation of the responses was assessed by use of valeryl salicylate (3 mM) and NS-398 (10 microM), inhibitors of COX-1 and COX-2, respectively. In eNOS-KO arterioles, valeryl salicylate or NS-398 alone inhibited FID (at maximal flow rate) by approximately 51% and approximately 58%, respectively. Administration of both inhibitors eliminated the dilation. In WT arterioles, inhibition of COX-2 did not significantly affect FID, whereas inhibition of COX-1 decreased the dilation by approximately 57%. The residual portion of the response was abolished by additional administration of Nomega-nitro-L-arginine methyl ester. Western blot ana...Continue Reading

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Citations

Jul 8, 2011·Journal of the Royal Society, Interface·Deshun Lu, Ghassan S Kassab
Feb 10, 2009·American Journal of Physiology. Heart and Circulatory Physiology·James L ParkJames A Shayman
Sep 24, 2011·American Journal of Physiology. Regulatory, Integrative and Comparative Physiology·Dong SunAn Huang
Feb 5, 2010·American Journal of Physiology. Regulatory, Integrative and Comparative Physiology·Dong SunAn Huang
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Nov 14, 2018·Frontiers in Pharmacology·An Huang, Dong Sun
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