Sildenafil and B-Type Natriuretic Peptide Acutely Phosphorylate Titin and Improve Diastolic Distensibility In Vivo | Zendy

Kalkidan Bishu | Zendy; Nazha Hamdani | Zendy; Selma F. Mohammed | Zendy; Martina Krüger | Zendy; Tomohito Ohtani | Zendy; Ozgur Ogut | Zendy; Frank V. Brozovich | Zendy; John C. Burnett | Zendy; Wolfgang A. Linke | Zendy; Margaret M. Redfield | Zendy

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Sildenafil and B-Type Natriuretic Peptide Acutely Phosphorylate Titin and Improve Diastolic Distensibility In Vivo

Author(s) -

Kalkidan Bishu,

Nazha Hamdani,

Selma F. Mohammed,

Martina Krüger,

Tomohito Ohtani,

Ozgur Ogut,

Frank V. Brozovich,

John C. Burnett,

Wolfgang A. Linke,

Margaret M. Redfield

Publication year - 2011

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.111.048520

Subject(s) - medicine , sildenafil , cardiology , titin , natriuretic peptide , troponin i , diastole , phospholamban , endocrinology , atrial natriuretic peptide , phosphorylation , myocyte , heart failure , blood pressure , sarcomere , myocardial infarction , chemistry , biochemistry

In vitro studies suggest that phosphorylation of titin reduces myocyte/myofiber stiffness. Titin can be phosphorylated by cGMP-activated protein kinase. Intracellular cGMP production is stimulated by B-type natriuretic peptide (BNP) and degraded by phosphodiesterases, including phosphodiesterase-5A. We hypothesized that a phosphodiesterase-5A inhibitor (sildenafil) alone or in combination with BNP would increase left ventricular diastolic distensibility by phosphorylating titin.

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