Manganese (0.5-100 mumol/l) was found to be a potent inhibitor of the dilator effect of isoprenaline on the isolated tracheal muscle of the guinea-pig. Above these concentrations the inhibitory action of Mn2+ diminished and no inhibition occurred above 1000 mumol/l Mn2+. Thus a bell-shaped dose-response curve resulted for the inhibition of isoprenaline by Mn2+. The antagonism was surmountable but apparently noncompetitive. Dilation of the isolated trachea caused by theophylline or nitroprusside was not inhibited by Mn2+ at concentrations of 12.5 to 750 mumol/l. At the dose range which could be tested manganese did not antagonize isoprenaline bronchodilatation in vivo. However, manganese at doses between 0.5 and 2.0 mumol/kg inhibited increased in pulmonary resistance caused by acetylcholine, histamine or serotonin. At concentrations above 250 mumol/l Mn2+ inhibited constrictor responses to histamine, acetylcholine and serotonin in guinea-pig isolated ileum and trachea, and inhibited serotonin and prostaglandin E2 contractions in rat fundus. Co2+, Fe2+, Fe3+ and Zn2+ were also tested for their action against isoprenaline on the isolated trachea. Co2+ was similar in effect to Mn2+ but had only 1/50 of the potency. Up to the highest concentrations which could be tested, namely 1000 mumol/l, the other trace metals produced negligible effects. Thus Mn2+ showed selective inhibition of the relaxant effect of isoprenaline on the guinea-pig isolated trachea, at concentrations of Mn2+ well below those shown previously to inhibit constrictor responses by block of transmembrane Ca2+ entry. It is suggested that Mn2+ may interfere with intracellular Ca2+ fluxes in the isolated trachea.
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