Open AccessNovel Nitric Oxide Donors Reverse Endothelin-1-Mediated Constriction in Human Blood Vessels
Author(s) -
Katherine Wiley,
Anthony P. Davenport
Publication year - 2000
Publication title -
journal of cardiovascular pharmacology
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 0.762
H-Index - 100
eISSN - 1533-4023
pISSN - 0160-2446
DOI - 10.1097/00005344-200036051-00047
Subject(s) - nitric oxide , snap , constriction , endothelin receptor , contraction (grammar) , endothelin 1 , potency , chemistry , pharmacology , in vitro , medicine , endocrinology , biochemistry , receptor , computer graphics (images) , computer science
Cardiovascular disease is associated with elevated circulating plasma levels of endothelin-1 (ET-1). Our aim was to compare the ability of the nitric oxide donors (NO-donors) 3-morpholinylsydnonimine (SIN-1) and S-nitroso-N-acetylpenicillamine (SNAP) with the novel nitric oxide donors (NONOates) diethylamine NONOate (DEA/NO), and diethylenetriamine NONOate (DETA/NO) in order to physiologically antagonize ET-1-mediated constriction of human internal mammary arteries (IMA) in vitro. Both SNAP and DETA/NO caused a significant rightward shift in the ET-1 concentration-response curve. All four NO-donors were found to completely reverse an established contraction to a submaximal concentration ET-1 (decreasing order potency: SNAP >DEA/NO > SIN-1 > DETA/NO). These data suggest that the NONOates DEA/NO and DETA/NO can physiologically antagonize the effects of ET-1 in human arteries and may prove to be useful therapeutic agents in the treatment of cardiovascular disease.