We examined agmatine and imidazoline derivatives as putative ligands of trimeric G protein in rat peritoneal mast cells. Agmatine induced a concentration-dependent and pertussis toxin-sensitive secretion of histamine (exocytosis) and arachidonate. Clonidine and idazoxan had no effect. Blockage of Gbetagamma dimers by a specific anti-Gbeta antibody inhibited exocytosis elicited by agmatine and mastoparan. The G protein antagonist [p-Glu(5),D-Trp(7,9,10)]substance P-(5-11) prevented both mastoparan- and agmatine-induced exocytosis when it was allowed to reach its intracellular targets by streptolysin-O permeabilisation. In intact cells, this response was prevented by both the removal of sialic acid residues by neuraminidase and by [D-Pro(4),D-Trp(7,9,10)]substance P-(4-11) acting at the mast cell surface. Exocytosis was restored by permeabilisation of the plasma membrane with streptolysin-O. These results suggest that agmatine might have several molecular targets, exerting its neurotransmitter function at low concentrations (i.e., with high affinity) through membrane receptors and at high concentrations (i.e., with weak affinity) through direct G protein activation.
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