Compounds > 1-1-diethyl-2-hydroxy-2-nitrosohydrazine

1-1-diethyl-2-hydroxy-2-nitrosohydrazine and phosphoramidon

1-1-diethyl-2-hydroxy-2-nitrosohydrazine has been researched along with phosphoramidon* in 1 studies

Other Studies

1 other study(ies) available for 1-1-diethyl-2-hydroxy-2-nitrosohydrazine and phosphoramidon

Article	Year
Increased endothelial exocytosis and generation of endothelin-1 contributes to constriction of aged arteries. Circulation research, 2010, Jul-23, Volume: 107, Issue:2 Circulating levels of endothelin (ET)-1 and endogenous ET(A)-mediated constriction are increased in human aging. The mechanisms responsible are not known.. Investigate the storage, release, and activity of ET-1 system in arteries from young and aged Fischer-344 rats.. After NO synthase inhibition (L-NAME), thrombin contracted aged arteries, which was inhibited by endothelial denudation, ET(A) receptor antagonism (BQ123), and ECE inhibition (phosphoramidon, SM19712) or by inhibiting exocytosis (TAT-NSF, N-ethylmaleimide-sensitive factor inhibitor). Thrombin did not cause endothelium-dependent contraction of young arteries. In aged but not young arteries, thrombin rapidly increased ET-1 release, which was abolished by endothelium denudation or TAT-NSF. L-NAME did not affect ET-1 release. ET-1 immunofluorescent staining was punctate and distinct from von Willebrand factor (VWF). VWF and ET-1 immunofluorescent intensity was similar in young and aged quiescent arteries. Thrombin rapidly increased ET-1 staining and decreased VWF staining in aged but had no effect in young aortas. After L-NAME, thrombin decreased VWF staining in young aortas. NO donor DEA-NONOate (1 to 100 nmol/L) reversed thrombin-induced exocytosis in young (VWF) but not aged L-NAME-treated aortas (VWF, ET-1). Expression of preproET-1 mRNA and ECE-1 mRNA were increased in aged compared to young endothelium. BigET-1 levels and contraction to exogenous BigET-1 (but not ET-1) were also increased in aged compared to young arteries.. The stimulated exocytotic release of ET-1 is dramatically increased in aged endothelium. This reflects increased reactivity of exocytosis, increased expression and storage of ET-1 precursor peptides, and increased expression of ECE-1. Altered endothelial exocytosis of ET-1 and other mediators may contribute to cardiovascular pathology in aging. Topics: Age Factors; Aging; Animals; Aorta, Thoracic; Aspartic Acid Endopeptidases; Dose-Response Relationship, Drug; Endothelin A Receptor Antagonists; Endothelin-1; Endothelin-Converting Enzymes; Enzyme Inhibitors; Exocytosis; Fluorescent Antibody Technique; Glycopeptides; Hydrazines; In Vitro Techniques; Mesenteric Arteries; Metalloendopeptidases; N-Ethylmaleimide-Sensitive Proteins; NG-Nitroarginine Methyl Ester; Nitric Oxide Donors; Nitric Oxide Synthase; Peptides, Cyclic; Rats; Rats, Inbred F344; Receptor, Endothelin A; RNA, Messenger; Sulfonamides; Sulfonylurea Compounds; Thrombin; Up-Regulation; Vasoconstriction; von Willebrand Factor	2010

Article

Year

Increased endothelial exocytosis and generation of endothelin-1 contributes to constriction of aged arteries.

Circulation research, 2010, Jul-23, Volume: 107, Issue:2

Circulating levels of endothelin (ET)-1 and endogenous ET(A)-mediated constriction are increased in human aging. The mechanisms responsible are not known.. Investigate the storage, release, and activity of ET-1 system in arteries from young and aged Fischer-344 rats.. After NO synthase inhibition (L-NAME), thrombin contracted aged arteries, which was inhibited by endothelial denudation, ET(A) receptor antagonism (BQ123), and ECE inhibition (phosphoramidon, SM19712) or by inhibiting exocytosis (TAT-NSF, N-ethylmaleimide-sensitive factor inhibitor). Thrombin did not cause endothelium-dependent contraction of young arteries. In aged but not young arteries, thrombin rapidly increased ET-1 release, which was abolished by endothelium denudation or TAT-NSF. L-NAME did not affect ET-1 release. ET-1 immunofluorescent staining was punctate and distinct from von Willebrand factor (VWF). VWF and ET-1 immunofluorescent intensity was similar in young and aged quiescent arteries. Thrombin rapidly increased ET-1 staining and decreased VWF staining in aged but had no effect in young aortas. After L-NAME, thrombin decreased VWF staining in young aortas. NO donor DEA-NONOate (1 to 100 nmol/L) reversed thrombin-induced exocytosis in young (VWF) but not aged L-NAME-treated aortas (VWF, ET-1). Expression of preproET-1 mRNA and ECE-1 mRNA were increased in aged compared to young endothelium. BigET-1 levels and contraction to exogenous BigET-1 (but not ET-1) were also increased in aged compared to young arteries.. The stimulated exocytotic release of ET-1 is dramatically increased in aged endothelium. This reflects increased reactivity of exocytosis, increased expression and storage of ET-1 precursor peptides, and increased expression of ECE-1. Altered endothelial exocytosis of ET-1 and other mediators may contribute to cardiovascular pathology in aging.

Topics: Age Factors; Aging; Animals; Aorta, Thoracic; Aspartic Acid Endopeptidases; Dose-Response Relationship, Drug; Endothelin A Receptor Antagonists; Endothelin-1; Endothelin-Converting Enzymes; Enzyme Inhibitors; Exocytosis; Fluorescent Antibody Technique; Glycopeptides; Hydrazines; In Vitro Techniques; Mesenteric Arteries; Metalloendopeptidases; N-Ethylmaleimide-Sensitive Proteins; NG-Nitroarginine Methyl Ester; Nitric Oxide Donors; Nitric Oxide Synthase; Peptides, Cyclic; Rats; Rats, Inbred F344; Receptor, Endothelin A; RNA, Messenger; Sulfonamides; Sulfonylurea Compounds; Thrombin; Up-Regulation; Vasoconstriction; von Willebrand Factor

2010