ArticleAmerican journal of physiology. Heart and circulatory physiology2009
Redox variants of NO (NO{middle dot} and HNO) elicit vasorelaxation of resistance arteries via distinct mechanisms.
Article in American journal of physiology. Heart and circulatory physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 74 citations in OpenAlex.
- NONO2P, a novel nitric oxide donor, causes vasorelaxation through NO/sGC/PKG pathway, KEuropean journal of pharmacology · 2024Article
- Redox Regulation of Mitochondrial Potassium Channels Activity.Antioxidants (Basel, Switzerland) · 2024Review
- Tracking endothelium-dependent NO release in pressurized arteries.Frontiers in physiology · 2023Article
- Cardiovascular Therapeutic Potential of the Redox Siblings, Nitric Oxide (NO•) and Nitroxyl (HNO), in the Setting of Reactive Oxygen Species Dysregulation.Handbook of experimental pharmacology · 2021Review
- An in vivo examination of the differences between rapid cardiovascular collapse and prolonged hypotension induced by snake venom.Scientific reports · 2019Article
- Advances in research on treatment of heart failure with nitrosyl hydrogen.Heart failure reviews · 2019Review
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- Article
- Perivascular Adipose Tissue-Enhanced Vasodilation in Metabolic Syndrome Rats by Apelin andInternational journal of molecular sciences · 2018Article
- Regulation of voltage-gated potassium channels in vascular smooth muscle during hypertension and metabolic disorders.Microcirculation (New York, N.Y. : 1994) · 2018Review
- Coronary microvascular Kv1 channels as regulatory sensors of intracellular pyridine nucleotide redox potential.Microcirculation (New York, N.Y. : 1994) · 2018Review
- Angeli's Salt, a nitroxyl anion donor, reverses endothelin-1 mediated vascular dysfunction in murine aorta.European journal of pharmacology · 2017Article
- Therapeutic Potential of Nitroxyl (HNO) Donors in the Management of Acute Decompensated Heart Failure.Drugs · 2016Review
- Hydrogen sulfide and endothelium-dependent vasorelaxation.Molecules (Basel, Switzerland) · 2014Review
- Ruthenium complexes as NO donors for vascular relaxation induction.Molecules (Basel, Switzerland) · 2014Review
- The concomitant coronary vasodilator and positive inotropic actions of the nitroxyl donor Angeli's salt in the intact rat heart: contribution of soluble guanylyl cyclase-dependent and -independent mechanisms.British journal of pharmacology · 2014Article
- Nitroxyl donors retain their depressor effects in hypertension.American journal of physiology. Heart and circulatory physiology · 2013Article
- Pharmacological characterization of 1-nitrosocyclohexyl acetate, a long-acting nitroxyl donor that shows vasorelaxant and antiaggregatory effects.The Journal of pharmacology and experimental therapeutics · 2013Article
- Endothelium-dependent nitric oxide and hyperpolarization-mediated venous relaxation pathways in rat inferior vena cava.Journal of vascular surgery · 2012Article
- Aorta from angiotensin II hypertensive mice exhibit preserved nitroxyl anion mediated relaxation responses.Pharmacological research · 2012Article
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2 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The free radical form of nitric oxide (NO(.)) is a well-known mediator of vascular tone. What is not so well recognized is that NO(.) exists in several different redox forms. There is considerable evidence that NO(.) and its one-electron reduction product, nitroxyl (HNO), have pharmacologically distinct actions that extend into the regulation of the vasculature. The aim of this study was to compare the vasorelaxation mechanisms of HNO and NO(.), including an examination of the ability of these redox variants to hyperpolarize and repolarize vascular smooth muscle cells from rat mesenteric arteries. The HNO donor Angeli's salt (0.1 nM-10 microM) caused a concentration-dependent hyperpolarization of vessels at resting tone and a simultaneous, concentration-dependent vasorelaxation and repolarization of vessels precontracted and depolarized with methoxamine. Both vasorelaxation and repolarization responses to Angeli's salt were significantly attenuated by both the HNO scavenger l-cysteine (3 mM) and the voltage-dependent K(+) (K(v)) channel inhibitor 4-aminopyridine (4-AP; 1 mM) and virtually abolished by the soluble guanylate cyclase (sGC) inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ; 10 microM) or 30 mM K(+). In contrast, NO(.) (0.01-1 microM) repolarized arteries to a lesser extent than HNO, and these responses were resistant to inhibition by ODQ (10 microM) and 4-AP (1 mM). Blockade of K(v) channels (1 mM 4-AP) also significantly inhibited the repolarization response to YC-1 (0.1-10 microM), confirming a role for sGC/cGMP in the activation of K(v) channels in this preparation. We conclude that HNO causes vasorelaxation via a cGMP-dependent activation of K(v) channels and that there are different profiles of vasorelaxant activity for the redox siblings HNO and NO(.).
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