Uncoupled Cardiac Nitric Oxide Synthase Mediates Diastolic Dysfunction | Zendy

Gad A. Silberman | Zendy; Tai-Hwang M. Fan | Zendy; Hong Liu | Zendy; Zhe Jiao | Zendy; Hong Xiao | Zendy; Joshua D. Lovelock | Zendy; Beth M. Boulden | Zendy; Julian D. Widder | Zendy; Scott Fredd | Zendy; Kenneth E. Bernstein | Zendy; Beata M. Wolska | Zendy; Sergey Dikalov | Zendy; David G. Harrison | Zendy; Samuel C. Dudley | Zendy

AI Assistant Blog Pricing

Home ZAIA Blog

Open Access

Uncoupled Cardiac Nitric Oxide Synthase Mediates Diastolic Dysfunction

Author(s) -

Gad A. Silberman,

Tai-Hwang M. Fan,

Hong Liu,

Zhe Jiao,

Hong Xiao,

Joshua D. Lovelock,

Beth M. Boulden,

Julian D. Widder,

Scott Fredd,

Kenneth E. Bernstein,

Beata M. Wolska,

Sergey Dikalov,

David G. Harrison,

Samuel C. Dudley

Publication year - 2010

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.109.883777

Subject(s) - phospholamban , diastole , medicine , endocrinology , nitric oxide synthase , heart failure , tetrahydrobiopterin , cardiology , cardiac output , ejection fraction , nitric oxide , blood pressure

Heart failure with preserved ejection fraction is 1 consequence of hypertension and is caused by impaired cardiac diastolic relaxation. Nitric oxide (NO) is a known modulator of cardiac relaxation. Hypertension can lead to a reduction in vascular NO, in part because NO synthase (NOS) becomes uncoupled when oxidative depletion of its cofactor tetrahydrobiopterin (BH(4)) occurs. Similar events may occur in the heart that lead to uncoupled NOS and diastolic dysfunction.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.

Having issues? You can contact us here

Accelerating Research