Activation of alpha-1A adrenoceptors mobilizes calcium from the intracellular stores in myocytes from rat portal vein
| Autor: | Lepretre, N, Mironneau, J., Arnaudeau, S, Tanfin, Z, Harbon, S, Guillon, G., Ibarrondo, J |
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| Přispěvatelé: | Laboratoire de Physiologie Cellulaire et Pharmacologie Moléculaire, INSERM CJF 88-13, Université de Bordeaux II, France., Archéologie, Terre, Histoire, Sociétés [Dijon] (ARTeHiS), Ministère de la Culture et de la Communication (MCC)-Université de Bourgogne (UB)-Centre National de la Recherche Scientifique (CNRS), Macrez, Nathalie, Centre National de la Recherche Scientifique (CNRS)-Université de Bourgogne (UB)-Ministère de la Culture et de la Communication (MCC) |
| Jazyk: | angličtina |
| Rok vydání: | 1994 |
| Předmět: |
Portal Vein
Inositol Phosphates [SDV]Life Sciences [q-bio] Molecular Sequence Data [SDV.BC]Life Sciences [q-bio]/Cellular Biology [SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC] In Vitro Techniques Antibodies Muscle Smooth Vascular Rats [SDV] Life Sciences [q-bio] Norepinephrine Chloride Channels Receptors Adrenergic alpha-1 [SDV.BC.BC] Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC] Animals Calcium Amino Acid Sequence Rats Wistar [SDV.BC] Life Sciences [q-bio]/Cellular Biology Adrenergic alpha-Antagonists Cells Cultured Signal Transduction |
| Zdroj: | Journal of Pharmacology and Experimental Therapeutics Journal of Pharmacology and Experimental Therapeutics, American Society for Pharmacology and Experimental Therapeutics, 1994, 268 (1), pp.167-74 HAL |
| ISSN: | 0022-3565 1521-0103 |
| Popis: | International audience; Intracellular free Ca++ concentration ([Ca++]i) was monitored using the fluorescence from the dye fura-2-acetoxymethylester in single myocytes from rat portal vein. In the presence of oxodipine (a L-type Ca++ channel inhibitor), norepinephrine (10 microM) evoked transient increases in [Ca++]i which were related to release of Ca++ from intracellular stores. The alpha-1 adrenoceptors mediating intracellular Ca++ release and inositol phosphate accumulation were identified by using subtype-selective agonists and antagonists. Pretreatment with chloroethylclonidine had little effect on the norepinephrine-induced increase in [Ca++]i and inositol phosphate accumulation. In contrast, prazosin, 2-(2,6-dimethoxyphenoxyethyl)aminomethyl-1,4-benzodioxane and alpha-ethyl-3,4,5-trimethoxy-alpha-(3-((2-(2-methoxyphenoxy)ethyl)-amino )- propyl)benzeneacetonitrile fumarate produced a concentration-dependent inhibition of both intracellular Ca++ release and inositol phosphate accumulation. The rank of potency was prazosin > 2-(2,6-dimethoxyphenoxyethyl)aminomethyl-1,4-benzodioxane > alpha-ethyl-3,4,5-trimethoxy-alpha-(3-((2-(2-methoxyphenoxy)ethyl)-amino - propyl) benzeneacetonitrile fumarate. Methoxamine was as effective as norepinephrine but was less potent as shown by the rightward shift of the concentration-response curves. These results indicate that myocytes from rat portal vein express alpha-1A adrenoceptors whose activation stimulates phosphoinositide turnover and release of Ca++ from intracellular stores. The alpha-1A adrenoceptor stimulation of [Ca++]i and subsequent activation of Ca(++)-activated Cl- current was insensitive to intracellular applications of pertussis toxin, but concentration-dependently blocked by intracellular dialysis with a pipette solution containing anti-alpha q/alpha 11 antibody (whole cell recording mode).(ABSTRACT TRUNCATED AT 400 WORDS) |
| Databáze: | OpenAIRE |
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