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• W2043286086 abstract "Until recently, most of the biological effects of nitric oxide (NO) have been attributed to its uncharged state (NO ), yet NO can also exist in the reduced state as nitroxyl (HNO or NO−). Putatively generated from both NO synthase (NOS)-dependent and -independent sources, HNO is rapidly emerging as a novel entity with distinct pharmacology and therapeutic advantages over its redox sibling, NO . Thus, unlike NO , HNO can target cardiac sarcoplasmic ryanodine receptors to increase myocardial contractility, can interact directly with thiols and is resistant to both scavenging by superoxide ( O2−) and tolerance development. HNO donors are protective in the setting of heart failure in which NO donors have minimal impact. Here, we discuss the unique pharmacology of HNO versus NO and highlight the therapeutic potential of HNO donors in the treatment of cardiovascular disease. Until recently, most of the biological effects of nitric oxide (NO) have been attributed to its uncharged state (NO ), yet NO can also exist in the reduced state as nitroxyl (HNO or NO−). Putatively generated from both NO synthase (NOS)-dependent and -independent sources, HNO is rapidly emerging as a novel entity with distinct pharmacology and therapeutic advantages over its redox sibling, NO . Thus, unlike NO , HNO can target cardiac sarcoplasmic ryanodine receptors to increase myocardial contractility, can interact directly with thiols and is resistant to both scavenging by superoxide ( O2−) and tolerance development. HNO donors are protective in the setting of heart failure in which NO donors have minimal impact. Here, we discuss the unique pharmacology of HNO versus NO and highlight the therapeutic potential of HNO donors in the treatment of cardiovascular disease. a small neuropeptide (37 amino acids) distributed throughout the central and peripheral nervous systems. CGRP is released from sensory nerves innervating the heart and coronary and peripheral arteries, and cardiovascular effects include vasodilation and positive cardiac inotropy (sympatho-stimulatory in nature). an agent that modulates the force of contraction of the heart; a positive cardiac inotrope increases myocardial contractility. myocardial injury and dysfunction following restoration of coronary blood flow after a period of ischaemia. a term to describe myocardial relaxation. an irreversible haem-site inhibitor of soluble guanylyl cyclase (sGC)." @default.
• W2043286086 created "2016-06-24" @default.
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• W2043286086 date "2008-12-01" @default.
• W2043286086 modified "2023-10-11" @default.
• W2043286086 title "Nitroxyl (HNO): the Cinderella of the nitric oxide story" @default.
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• W2043286086 doi "https://doi.org/10.1016/j.tips.2008.08.005" @default.
• W2043286086 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/18835046" @default.
• W2043286086 hasPublicationYear "2008" @default.
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