Evidence that calcium acts as an intracellular messenger for adrenergic responses in human erythrocytes.
Adrenergic stimulation of membrane protein phosphorylation has been studied in human erythrocytes. The adrenergic enhancement in phosphorylation of band 2 could be mimicked by the calcium-specific ionophore A23187 in the presence of 10 micron extracellular calcium. Experiments with the potassium ionophore, valinomycin, showed that potassium efflux was not the primary effector of the response. Trifluoperazine, an inhibitor of the Ca2+-dependent regulatory protein, calmodulin, inhibited phosphorylation stimulation by either norepinephrine or the calcium ionophore. The norepinephrine response was observed in the absence of extracellular calcium, implicating Ca2+ released from cellular bound pools in mediating the response.
D000001:Calcimycin; D002118:Calcium / Q000097:blood*; D004533:Egtazic Acid / Q000494:pharmacology; D004910:Erythrocyte Membrane / Q000378:metabolism; D004912:Erythrocytes / Q000187:drug effects / Q000378:metabolism*; D006801:Humans; D008565:Membrane Proteins / Q000097:blood; D009638:Norepinephrine / Q000494:pharmacology*; D010766:Phosphorylation; D013049:Spectrin / Q000378:metabolism; D014268:Trifluoperazine / Q000494:pharmacology*; D014634:Valinomycin / Q000494:pharmacology
D008565:Membrane Proteins; D013049:Spectrin; D014634:Valinomycin; D014268:Trifluoperazine; D000001:Calcimycin; D004533:Egtazic Acid; D002118:Calcium; D009638:Norepinephrine