2000
DOI: 10.1073/pnas.97.17.9747
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An endothelium-derived hyperpolarizing factor distinct from NO and prostacyclin is a major endothelium-dependent vasodilator in resistance vessels of wild-type and endothelial NO synthase knockout mice

Abstract: In addition to nitric oxide (NO) and prostacyclin (PGI2), the endothelium generates the endothelium-derived hyperpolarizing factor (EDHF). We set out to determine whether an EDHF-like response can be detected in wild-type (WT) and endothelial NO synthase knockout mice (eNOS ؊͞؊) mice. Vasodilator responses to endothelium-dependent agonists were determined in vivo and in vitro. In vivo, bradykinin induced a pronounced, dose-dependent decrease in mean arterial pressure (MAP) which did not differ between WT and e… Show more

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Cited by 255 publications
(222 citation statements)
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References 37 publications
(35 reference statements)
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“…Moreover, the efficacy of NO as well as ACh in reducing pressure were similar in both wild-type and Cx40 Ϫ/Ϫ mice, suggesting that the dilator potency of enhanced levels of NO is also not affected by the loss of Cx40. Recently, it has been proposed that dilations induced by ACh in mice involve a mechanism that is distinct from NO and prostaglandins (2). Also in the present study, systemic blockade of NO synthase did not affect the maximal amplitude, but only the duration of ACh-induced pressure drops, suggesting that other endothelial dilator mechanisms, namely endothelium-derived hyperpolarizing factor (EDHF), are important.…”
Section: Discussionsupporting
confidence: 46%
See 1 more Smart Citation
“…Moreover, the efficacy of NO as well as ACh in reducing pressure were similar in both wild-type and Cx40 Ϫ/Ϫ mice, suggesting that the dilator potency of enhanced levels of NO is also not affected by the loss of Cx40. Recently, it has been proposed that dilations induced by ACh in mice involve a mechanism that is distinct from NO and prostaglandins (2). Also in the present study, systemic blockade of NO synthase did not affect the maximal amplitude, but only the duration of ACh-induced pressure drops, suggesting that other endothelial dilator mechanisms, namely endothelium-derived hyperpolarizing factor (EDHF), are important.…”
Section: Discussionsupporting
confidence: 46%
“…avi) and is also available as Supplementary Material at the Physiological Genomics web site]. 2 When observed in an arteriole, these constrictions could be abrogated by the superfusion of ACh or SNP but returned upon removal of the dilator substance. In contrast to this irregular behavior, normal vasomotion is characterized by simultaneous diameter changes along the entire vessel length and can be observed in wildtype and Cx40-deficient mice (Fig.…”
Section: Responses To Endothelium-dependent and -Independent Vasodilamentioning
confidence: 99%
“…8 EDHF is a non-NO, non-prostanoid endothelium-derived hyperpolarizing factor that persists after effective inhibition of nitric oxide synthase and cyclo-oxygenase pathways. 9,10 EDHF dependent vasorelaxation is mediated through calcium-activated potassium channels (KCa). 11 Several substances may comprise EDHF, including epoxyeicosatrienoic acid (EET), anandamide, hydrogen peroxide, and potassium ion.…”
mentioning
confidence: 99%
“…16,32 In contrast, the present study documented that overexpression of Flk-sel reduced systemic BP, despite eNOS deficiency. This suggests that alternative factors that contribute to BP regulation, including endothelial-derived hyperpolarizing factor, [47][48][49][50] could be altered by Flk-sel.…”
Section: Discussionmentioning
confidence: 99%