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Thus, we found that mesenteric arterioles of homozygous mice (GPx1 −/− ) and older heterozygous (GPx1 +/− ) knockout mice had a loss of NO-dependent vasodilatory responses to β- methacholine and bradykinin, instead showing a vasoconstrictor response to these mediators that cause vasodilation in wildtype arterioles [39, 71]
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