Catecholamines-evoked cytosolic Ca2+ rise in endothelial cells from bovine adrenal medulla.
The effects of catecholamines on intracellular Ca2+ concentrations ([Ca2+]i) in single acutely dissociated bovine adrenal medulla endothelial cells (BAMECs) were measured using the intracellular fluorescent probe Fluo-3 AM. 100 microm epinephrine or norepinephrine induced a biphasic [Ca2+]i rise with an initial peak followed by a delayed phase. 10 microm phenylephrine (alpha1-adrenergic agonist) caused a [Ca2+]i rise similar to that evoked by catecholamines. The increase in [Ca2+]i induced by 10 microm phenylephrine was reverted by 10 microm phenoxybenzamine (alpha-adrenergic antagonist). Neither isoproterenol (beta-adrenergic agonist) nor clonidine (alpha2-adrenergic agonist) induced [Ca2+]i rise. The initial peak was insensitive to zero external Ca2+ and it was abolished after Ca2+ internal storages were emptied by 10 mM caffeine. The delayed phase was reduced to near zero by external Ca2+ removal. These results indicate that BAMECs possess alpha1-adrenergic receptors associated to both the release of caffeine-sensitive intracellular Ca2+ stores and the entry of extracellular Ca2+. We suggest that chromaffin cell secretion may activate BAMECs in vivo through an increase in [Ca2+]i which could induce the secretion of vasoactive factors allowing a rapid entry of hormones into the circulation.
Vinet
R
R
Escuela de Quimica y Farmacia, Facultad de Medicina, Universidad de Valparaiso, Chile.
Rojas
F
F
Luxoro
M
M
Vargas
F
F
Cortés
M
M
D000313:Adrenal Medulla / Q000187:drug effects* / Q000378:metabolism; D058646:Adrenergic alpha-1 Receptor Agonists; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002395:Catecholamines / Q000494:pharmacology*; D002417:Cattle; D003600:Cytosol / Q000187:drug effects / Q000378:metabolism; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000378:metabolism
D058646:Adrenergic alpha-1 Receptor Agonists; D002395:Catecholamines; D002118:Calcium