Disruption of Physiological Balance Between Nitric Oxide and Endothelium-Dependent Hyperpolarization Impairs Cardiovascular Homeostasis in Mice | Zendy

Shigeo Godo | Zendy; Ayuko Sawada | Zendy; Hiroki Saito | Zendy; Shohei Ikeda | Zendy; Budbazar Enkhjargal | Zendy; Kota Suzuki | Zendy; Shuhei Tanaka | Zendy; Hiroaki Shimokawa | Zendy

Open Access

Disruption of Physiological Balance Between Nitric Oxide and Endothelium-Dependent Hyperpolarization Impairs Cardiovascular Homeostasis in Mice

Author(s) -

Shigeo Godo,

Ayuko Sawada,

Hiroki Saito,

Shohei Ikeda,

Budbazar Enkhjargal,

Kota Suzuki,

Shuhei Tanaka,

Hiroaki Shimokawa

Publication year - 2015

Publication title -

arteriosclerosis thrombosis and vascular biology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.007

H-Index - 270

eISSN - 1524-4636

pISSN - 1079-5642

DOI - 10.1161/atvbaha.115.306499

Subject(s) - enos , medicine , endocrinology , nitric oxide , endothelium , knockout mouse , homeostasis , endothelial dysfunction , mesenteric arteries , chemistry , nitric oxide synthase , biology , artery , receptor

Endothelium-derived nitric oxide (NO) and endothelium-dependent hyperpolarization (EDH) play important roles in modulating vascular tone in a distinct vessel size-dependent manner; NO plays a dominant role in conduit arteries and EDH in resistance vessels. We have recently demonstrated that endothelial NO synthase (eNOS) is functionally suppressed in resistance vessels through caveolin-1 (Cav-1)-dependent mechanism, switching its function from NO to EDH/hydrogen peroxide generation in mice. Here, we examined the possible importance of the physiological balance between NO and EDH in cardiovascular homeostasis.

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