Role of Endothelial Nitric Oxide and Smooth Muscle Potassium Channels in Cerebral Arteriolar Dilation in Response to Acidosis | Zendy

Tetsuyoshi Horiuchi | Zendy; Hans H. Dietrich | Zendy; Kazuhiro Hongo | Zendy; Tetsuya Goto | Zendy; Ralph G. Dacey | Zendy

Open Access

Role of Endothelial Nitric Oxide and Smooth Muscle Potassium Channels in Cerebral Arteriolar Dilation in Response to Acidosis

Author(s) -

Tetsuyoshi Horiuchi,

Hans H. Dietrich,

Kazuhiro Hongo,

Tetsuya Goto,

Ralph G. Dacey

Publication year - 2002

Publication title -

stroke

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.397

H-Index - 319

eISSN - 1524-4628

pISSN - 0039-2499

DOI - 10.1161/hs0302.104112

Subject(s) - glibenclamide , nitric oxide , potassium channel , medicine , endocrinology , acidosis , nitric oxide synthase , vascular smooth muscle , potassium , chemistry , organic chemistry , diabetes mellitus , smooth muscle

Potassium channels or nitric oxide or both are major mediators of acidosis-induced dilation in the cerebral circulation. However, these contributions depend on a variety of factors such as species and vessel location. The present study was designed to clarify whether potassium channels and endothelial nitric oxide are involved in acidosis-induced dilation of isolated rat cerebral arterioles.

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