1The effect of ouabain on the histamine secretion induced by compound 48/80 has been studied using rat peritoneal mast cells.

The inhibition of sodium-potassium ATPase by ouabain or potassium-deprivation led to a potentiation of histamine release induced by antigen or compound 48/80 from rat mast cells. The fullest potentiation required 30 min preincubation of cells with ouabain or without potassium before adding the triggering agent. The potentiation was observed provided that the calcium concentration was less than 0.5 mM. The effect of sodium-potassium ATPase blockade was reversed slowly by washing out ouabain or by adding potassium. Metabolic inhibition with deoxyglucose and dinitrophenol-blocked histamine release observed under all conditions described. Histamine release from rat mast cells was also elicited when the cells were incubated in sodium-deficient media where sodium was replaced by sucrose. Potassium-deprivation potentiated this secretion process previously shown to be dependent upon metabolic energy and sensitive to millimolar calcium concentrations.

Clenbuterol 10(-8) to 10(-6) M inhibited antigen-induced histamine release from passively sensitized human lung tissue. This inhibition was not antagonized by propranolol, whereas the inhibitions observed with isoprenaline and fenoterol were reduced by propranolol. Clenbuterol also inhibited compound 48/80-induced histamine release and immunological histamine secretion from actively sensitized peritoneal rat mast cells. High concentrations of clenbuterol were required (10(-5) to 10(-3) M) and propranolol did not antagonize these inhibitions of histamine release. Isoprenaline and salbutamol did not modify the secretion from rat mast cells. The potential anti-anaphylactic activity of clenbuterol, might be partly related to its calcium antagonist property.