Functional involvement of α1and α2-adrenoceptors in86Rb efflux from liver slices and lipolysis in guinea-pig isolated adipocytes
Autor: | Rosario Maroto, Consuelo Sancho, Julio Moratinos |
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Rok vydání: | 1992 |
Předmět: |
Male
Agonist medicine.medical_specialty Epinephrine medicine.drug_class Lipolysis Guinea Pigs Alpha (ethology) chemistry.chemical_element In Vitro Techniques Calcium Biology Apamin Amidephrine chemistry.chemical_compound Internal medicine Isoprenaline medicine Prazosin Animals Adrenergic alpha-Antagonists Pharmacology General Neuroscience Isoproterenol Receptors Adrenergic alpha Liver Glycogen Yohimbine Glucose Endocrinology Adipose Tissue Liver chemistry Adrenergic alpha-Agonists Rubidium Radioisotopes medicine.drug |
Zdroj: | Journal of Autonomic Pharmacology. 12:277-290 |
ISSN: | 1365-2680 0144-1795 |
DOI: | 10.1111/j.1474-8673.1992.tb00377.x |
Popis: | 1. The application of an alpha 1-adrenoceptor agonist, amidephrine, to guinea-pig liver slices increases glucose release and 86Rb efflux. Since prazosin was more potent than yohimbine in inhibiting both responses, alpha 1-adrenoceptors seem to be involved in the effects evoked by the agonist. 2. Clonidine (an alpha 2-adrenoceptor agonist) at doses unable to activate liver glycogenolysis increased 86Rb release and potentiated isoprenaline in promoting 86Rb efflux. Since yohimbine antagonized clonidine in promoting 86Rb efflux, alpha 2-adrenoceptors also seem to control plasmalemmal permeability to 86Rb. 3. The liver slice responses resulting from alpha 1- and alpha 2-adrenoceptor stimulation required extracellular calcium. Calcium absence or the administration of D-600 attenuated the effects of amidephrine on glucose release and 86Rb outflow and Ca2+ excess re-established both responses. D-600 and apamin blocked clonidine-induced 86Rb efflux, suggesting that alpha 2-adrenoceptor stimulation activates calcium dependent K+ channels. 4. alpha 2-adrenoceptors do not appear to mediate antilipolytic effects in guinea-pig fat cells. |
Databáze: | OpenAIRE |
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