Research paperNitric oxide (NO•), the only nitrogen monoxide redox form capable of activating soluble guanylyl cyclase☆
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Cited by (96)
Nitric oxide resistance in type 2 diabetes: Potential implications of HNO donors
2023, Nitric Oxide in Health and Disease: Therapeutic Applications in Cancer and Inflammatory DisordersActivation of soluble guanylyl cyclase with inhibition of multidrug resistance protein inhibitor-4 (MRP4) as a new antiplatelet therapy
2018, Biochemical PharmacologyCitation Excerpt :Interestingly, MK 571 alone, at a threshold concentration (10 µM) did not interfere on platelet function, implying that its action is favored with BAY 60-2770-stimulating cGMP levels. Soluble guanylate cyclase (sGC) is the major intracellular receptor for endogenous and exogenous NO [31] as well as for sGC modulators [32]. It has been shown that increased levels of oxidative stress in vascular-related diseases lead to oxidation or even loss of the sGC haem group, leading the enzyme insensitive to NO [8].
Nitrite potentiates the vasodilatory signaling of S-nitrosothiols
2018, Nitric Oxide - Biology and ChemistryThe Interaction of HNO With Transition Metal Centers and Its Biological Significance. Insight Into Electronic Structure From Theoretical Calculations
2017, The Chemistry and Biology of Nitroxyl (HNO)Recent advances in the chemical biology of nitroxyl (HNO) detection and generation
2016, Nitric Oxide - Biology and ChemistryCitation Excerpt :These initial findings triggered wide-ranging investigations to support and explore NO-based physiological signaling [4,7,8]. For example, metallo-heme proteins, particularly soluble guanylate cyclase (sGC) in terms of smooth muscle relaxation, were identified as valid biological targets of NO that ultimately allowed the development of new clinical phosphodiesterase inhibitors that modulate NO's actions [4,5,9–12]. Protein thiols react with NO or its redox forms to yield S-nitrosothiols (RSNO) that control NO transport, preservation and form an NO-based post-translational modification [13,14].
Local and systemic vasodilatory effects of low molecular weight S-nitrosothiols
2016, Free Radical Biology and MedicineCitation Excerpt :These results are consistent with a previous report that L-cysNO has stronger hypotensive effects than D-cysNO in the conscious rat [3]. SNOs are proposed to mediate vasodilation by activation of sGC within vascular smooth muscle cells [12,30–33], although direct effects of SNOs on ion channels such as large-conductance Ca2+-activated K+ channels have also been reported [14,34]. sGC activation requires intracellular NO [12,30–33], and several pathways by which extracellular SNOs are converted into intracellular NO have been proposed.
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This research was supported by a Grant-in-Aid from the American Heart Association. E.A.D. gratefully acknowledges support of the NIH Biotechnology Training Grant.
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In partial fulfillment of the requirements for the Ph.D., June 1995.