The sensitivity of adrenergic varicosities to the 3H-noradrenaline-releasing effect of potassium.

After the loading of incubated, homogeneously innervated tissues with 3H-noradrenaline (monoamine oxidase and catechol-O-methyl transferase inhibited, calcium-containing solution) high K+ released the 3H-amine from adrenergic varicosities. In paired experiments the sensitivity of rat atria to high K+ exceeded that of vasa deferentia. In the rat vas deferens the releasing effect of high K+ was enhanced by drugs or procedures which induce a carrier-mediated outward transport of 3H-noradrenaline, i.e., by ouabain, by glucose deprivation and by hypoxia. In the presence of extracellular calcium desipramine failed to affect the releasing effect of high K+ (except in the absence of glucose or during hypoxia), but in the absence of calcium desipramine reduced it. Apparently, whenever the axoplasmic levels of 3H-noradrenaline are increased, high K+ is able to induce some carrier-mediated outward transport of the 3H-amine. It is suggested that "organ differences" with respect to the sensitivity to high K+ may well be due to hypoxia (plus some lack of glucose) of those varicosities that had been loaded with 3H-noradrenaline. The risk of storage of 3H-noradrenaline in hypoxic varicosities appears to be greater in incubated than in perfused organs, and in the former it is greater in sparsely than in densely innervated tissues.