作者: Sidsel Aardal , Karen B. Helle , Said Elsayed , Rolf K. Reed , Guldborg Serck-Hanssen
DOI: 10.1111/J.1365-2826.1993.TB00501.X
关键词: Internal medicine 、 Chromogranin A 、 Blood vessel 、 Endothelin 1 、 Contraction (grammar) 、 Chemistry 、 Muscle contraction 、 Peptide hormone 、 Nifedipine 、 Receptor 、 Endocrinology
摘要: Chromogranin A (CGA) belongs to a family of highly acidic proteins which are co-stored and co-released with the catecholamines from mammalian adrenal gland occur in nmolar concentrations human circulation. vascular function for adrenomedullary released circulating CGA has yet be established. The present study reports on novel vasoinhibitory effect N-terminal domain isolated segments internal thoracic artery (ITA) saphenous vein (SV). collective term vasostatin(s) refers fragments (CGA1–76 CGA1–113) apparent molecular weights 7 22 kD, indicate their inhibitory effects. sustained contractions evoked by potent vasoconstrictor peptide, endothelin-1 (ET-1) were suppressed when ITA SV preincubated 15 min vasostatins (72 nM). effects not dependent an intact endothelium suppression response 35 nM ET-1 was ∼77% ∼40% endothelium-denuded segments, respectively. In maximal tension but potency ET-1, indicating that vasostatin did involve interference binding its receptor. Preincubation nifedipine (1 μM) inhibited ≥10 50%. By same protocol 20 40% contraction obtained nM), suggesting inhibition Ca2 channel opening might indirectly contribute ET-1. mechanisms these blood vessels remain elucidated.