Nitroglycerin Fails to Lower Blood Pressure in Redox-Dead Cys42Ser PKG1α Knock-In Mouse | Zendy

Olena Rudyk | Zendy; Oleksandra Prysyazhna | Zendy; Joseph R. Burgoyne | Zendy; Philip Eaton | Zendy

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Nitroglycerin Fails to Lower Blood Pressure in Redox-Dead Cys42Ser PKG1α Knock-In Mouse

Author(s) -

Olena Rudyk,

Oleksandra Prysyazhna,

Joseph R. Burgoyne,

Philip Eaton

Publication year - 2012

Publication title -

circulation

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 7.795

H-Index - 607

eISSN - 1524-4539

pISSN - 0009-7322

DOI - 10.1161/circulationaha.112.101287

Subject(s) - vasodilation , nitric oxide , in vivo , redox , pharmacology , nitroglycerin (drug) , knockout mouse , chemistry , endocrinology , medicine , anesthesia , biology , receptor , microbiology and biotechnology , organic chemistry

Although nitroglycerin has remained in clinical use since 1879, the mechanism by which it relaxes blood vessels to lower blood pressure remains incompletely understood. Nitroglycerin undergoes metabolism that generates several reaction products, including oxidants, and this bioactivation process is essential for vasodilation. Protein kinase G (PKG) mediates classic nitric oxide-dependent vasorelaxation, but the 1α isoform is also independently activated by oxidation that involves interprotein disulfide formation within this homodimeric protein complex. We hypothesized that nitroglycerin-induced vasodilation is mediated by disulfide activation of PKG1α.

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