Abstract
C2 synthesis by monocytes is stimulated by carbamylcholine acting on nicotinic receptors, phenylephrine acting on alpha 1 adrenergic receptors, and antigen-antibody complexes (IC) acting on Fc receptors. Stimulation of C2 synthesis is reversed by agents which block calcium (LaCl2, CoCl2, verapamil, nifedipidine, diltiazem) and sodium channels (tetrodotoxin) and calmodulin antagonists (trifluoperazine and W7). The changes in intracellular cyclic nucleotide levels that follow these receptor-ligand interactions (decreased cAMP, increased cGMP) do not occur in the presence of calcium and sodium channel blockers. These results suggest that the transmembrane signal which is involved in the stimulation of C2 synthesis is the entry of sodium and calcium ions. Whether this influx occurs by separate channels or a common channel has not been determined. The intracellular events involved in the stimulation of C2 synthesis appear to be calmodulin-dependent.
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Selected References
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