Barium and strontium can substitute for calcium in noradrenaline output induced by excess potassium in the guinea‐pig.

Abstract

The ability of Ba2+ and Sr2+ to substitute for Ca2+ in the noradrenaline [norepinephrine, NE] output induced by excess K+ was examined using isolated guinea-pig vas deferens. When the vas deferens was repeatedly exposed to excess K+ (60 mM) at 40 min intervals, the NE output increased at least 3-fold in incubation medium, which contained either Ca2+, Ba2+ or Sr2+. The response decreased on repetition. The order of effectiveness was roughly Ba2+ > Ca2+ > Sr2+. In the absence of excess K+, these cations had no significant stimulating effect on the NE output even when added after exposure to Ca2+-free solution. As the concentration of divalent cation was increased from 0.2-2.5 mM the NE output induced by excess K+ increased. The maximum NE output was achieved at a divalent cation concentration of 2.5 mM and was 29.56 .+-. 3.52, 15.02 .+-. 1.12 and 7.45 .+-. 0.84 (mean .+-. SE of mean) nmol/g per h in the presence of either Ba2+, Ca2+ or Sr2+, respectively. Further increase in the concentration of the cations reduced the response. The addition of either Sr2+ (2 mM) or Ca2+ (1 mM) to a solution containing various concentrations of Ba2+ facilitated the K+-induced increase in the NE output when the Ba2+ concentration was low, but inhibited release of NE when higher concentrations of Ba2+ were used. The addition of (1 mM) to Ca2+-containing solutions had a similar effect. Mg2+ competitively inhibited the K+-induced increase in the NE output in the presence of either Ba2+ or Sr2+ and blocked that in the presence of Ca2+. Apparently, both Ba2+ and Sr2+ can substitute for Ca2+ in the release of NE at adrenergic nerve terminals. It seems likely that all these cations act through the same site at some stage in the process of K+-induced transmitter release.