2003
DOI: 10.1152/ajplung.00133.2003
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Hypoxic regulation of nitric oxide signaling in vascular smooth muscle

Abstract: THE CURRENT ARTICLE IN FOCUS by Mingone and colleagues (Ref. 16, see p. L296 in this issue) describes a novel permissive effect of hypoxia on cGMP-independent relaxation to nitric oxide (NO) in bovine pulmonary and coronary arteries. Interestingly, whereas NO-mediated vasorelaxation appeared to be largely a function of cGMP at ambient PO 2 , a cGMP-independent mechanism involving activation of the sarco(endo)plasmic reticulum Ca 2ϩ -ATPase (SERCA) was revealed during hypoxic exposure. This study emphasizes the… Show more

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Cited by 2 publications
(4 citation statements)
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“…3 . Signal transduction of NO• in VSM involves two major pathways: (1) the indirect pathway of NO•-sGC-cGMP-PKG [ 128 , 150 , 151 ] and (2) the direct pathway of protein S -nitrosylation [ 128 , 150 , 151 ], also called cGMP-dependent and -independent pathways, respectively [ 152 ] ( Fig. 3 ) .…”
Section: No• Actions In Vsm In Normal Conditions and T2dmentioning
confidence: 99%
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“…3 . Signal transduction of NO• in VSM involves two major pathways: (1) the indirect pathway of NO•-sGC-cGMP-PKG [ 128 , 150 , 151 ] and (2) the direct pathway of protein S -nitrosylation [ 128 , 150 , 151 ], also called cGMP-dependent and -independent pathways, respectively [ 152 ] ( Fig. 3 ) .…”
Section: No• Actions In Vsm In Normal Conditions and T2dmentioning
confidence: 99%
“…3 ) . Although both pathways are found in the VSM, NO•-mediated vasorelaxation is mostly cGMP-dependent at a normal oxygen pressure [ 152 ]. The NO• concentrations eliciting a physiological response in VSM have been estimated to fall from 100 pM to 5 nM [ 153 ].…”
Section: No• Actions In Vsm In Normal Conditions and T2dmentioning
confidence: 99%
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“…However, when • NO complexes with thiol groups to form RSNO, it increases the life span by protecting the • NO from inactivation by metalloproteins (especially hemoglobin) and free radicals (especially superoxide and lipid peroxyl radical). RSNO can elicit their biological activity by releasing • NO, resulting in the activation of the classical guanylyl cyclase-/cGMP-dependent pathway or the cGMP-independent pathway, which includes post-translational modification of proteins [3–7]. RSNO are potent vasodilators [8, 9], strong inhibitors of platelet aggregation [10, 11] and leukocyte binding to the vascular endothelium [12–14].…”
Section: Introductionmentioning
confidence: 99%