6533b851fe1ef96bd12a8e09

RESEARCH PRODUCT

Effects of endothelin-1 on the cerebrovascular bed of the goat.

Enrique AlborchJuan B. SalomGermán TorregrosaFrancisco J. MirandaCristina AlvarezJoséa. Alabadí

subject

medicine.medical_specialtyEndotheliumCerebral arteriesNicardipineIn Vitro TechniquesMuscle Smooth VascularCerebral circulationNicardipineInternal medicinemedicine.arteryIsometric ContractionmedicineAnimalsPharmacologyChemistryCalcium RadioisotopesEndothelinsGoatsAnatomy3-Pyridinecarboxylic acid 14-dihydro-26-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)- Methyl esterEndothelin 1Acetylcholinemedicine.anatomical_structureEndocrinologyCerebral blood flowCerebrovascular CirculationMiddle cerebral arteryPotassiumCalciumFemaleBlood vesselmedicine.drug

description

Abstract The aim of the present study was to analyze the effects of endothelin-1 (ET-1) in the cerebrovascular bed of the goat, the importance of endothelial integrity and the contribution of extracellular Ca2+ to these responses. We measured isometric tension and 45Ca2+ uptake in isolated middle cerebral arteries, and cerebral blood flow (CBF) in unanesthetized animals. ET-1 elicited concentration-dependent contractions which were potentiated in arteries without endothelium. Ca2+-free medium and nicardipine inhibited, and Bay K 8644 potentiated the ET-1-induced contractions. ET-1 enhanced 45Ca2+ uptake in isolated arteries. Injections of ET-1 directly into the cerebral circulation decreased CBF and increased cerebrovascular resistance in a dose-dependent manner. Infusion of nicardipine inhibited the ET-1-induced reductions in CBF. These results suggest that ET-1 reduces CBF of goats because of contraction of cerebral arteries by a direct action on smooth muscle, which is modulated by the endothelium and depends partially on the activation of Ca2+ influx through dihydropyridine-sensitive channels.

10.1016/0014-2999(91)90066-yhttps://pubmed.ncbi.nlm.nih.gov/1710188