Loss of receptor-mediated 86Rb efflux from pig aortic endothelial cells in culture.
The responsiveness of freshly-isolated and subcultured pig aortic endothelial cells to adenosine triphosphate (ATP), bradykinin and ionophore A23187 was compared by monitoring agonist-induced 86Rb efflux. ATP, bradykinin and ionophore A23187 stimulated 86Rb efflux from freshly-isolated cells. ATP and bradykinin, which act via specific receptors, were less effective at inducing 86Rb efflux from subcultured cells but ionophore A23187 was as effective on subcultured as on freshly-isolated cells. These results suggest that pig aortic endothelial cells, when subcultured, lose receptors for ATP and bradykinin and/or develop an abnormality in the coupling-mechanism between receptor-occupation and calcium-mobilization.
D000255:Adenosine Triphosphate / Q000494:pharmacology; D000818:Animals; D001920:Bradykinin / Q000494:pharmacology; D000001:Calcimycin / Q000494:pharmacology*; D004727:Endothelium / Q000187:drug effects / Q000378:metabolism; D066298:In Vitro Techniques; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000378:metabolism*; D011868:Radioisotopes; D018002:Receptors, Bradykinin; D011956:Receptors, Cell Surface / Q000378:metabolism; D011983:Receptors, Purinergic; D012413:Rubidium / Q000378:metabolism*; D013552:Swine
D011868:Radioisotopes; D018002:Receptors, Bradykinin; D011956:Receptors, Cell Surface; D011983:Receptors, Purinergic; D000001:Calcimycin; D000255:Adenosine Triphosphate; D012413:Rubidium; D001920:Bradykinin