The energy requirements for the basal efflux of 3H-noradrenaline from sympathetically innervated organs.
In the rat vas deferens (preloaded with 3H-noradrenaline, catechol-O-methyl transferase inhibited, calcium-free solution) ouabain, glucose deprivation or the combination of hypoxia plus presence of lactate were found to induce a carrier-mediated (desipramine-sensitive) outward transport of the 3H-amine. Glucose deprivation additionally increased the efflux of deaminated 3H-metabolites, as a consequence of an increased net leakage of vesicular 3H-noradrenaline; moreover, 3H-dihydroxymandelic acid then became the predominant neuronal metabolite. The simultaneous lack of oxygen and glucose resulted in a very pronounced release of the 3H-amine. Moreover, during spontaneous efflux more outward transport of 3H-noradrenaline was observed in the absence than in the presence of extracellular calcium. In rat atria (under the same experimental conditions) the contribution by carrier-mediated outward transport to the spontaneous efflux of tritium exceeded that in vasa deferentia. Moreover, the efflux of lactate (as an index of hypoxia of the tissue) exceeded that observed in vasa deferentia, under aerobic and anaerobic conditions. It is proposed that the greater contribution by outward transport of 3H-noradrenaline to spontaneous efflux in atria than in vasa deferentia does not reflect any basic difference between the varicosities in two different organs. It is likely that the less heterogeneous distribution of the 3H-amine in atria than in vasa deferentia is responsible for storage of the exogenous amine in atrial varicosities that are subject to some hypoxia, to an increased extracellular lactate level and to perhaps a minor degree of glucose deficiency; these factors may well be responsible for the difference with regard to outward transport of 3H-noradrenaline during spontaneous efflux. Thus, in addition to the heterogeneity of the distribution of 3H-noradrenaline, an additional heterogeneity with regard to the energy supply must be expected for incubated organs.
Russ
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H
Institut für Pharmakologie und Toxikologie, Universität Würzburg, Federal Republic of Germany.
Schömig
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E
Trendelenburg
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U
D000818:Animals; D016275:Atrial Function; D001692:Biological Transport; D002118:Calcium / Q000494:pharmacology; D065098:Catechol O-Methyltransferase Inhibitors; D003891:Desipramine / Q000494:pharmacology; D004734:Energy Metabolism; D005110:Extracellular Space / Q000378:metabolism; D005947:Glucose / Q000172:deficiency / Q000494:pharmacology; D006325:Heart Atria / Q000294:innervation; D000860:Hypoxia / Q000378:metabolism / Q000503:physiopathology; D066298:In Vitro Techniques; D007773:Lactates / Q000096:biosynthesis / Q000494:pharmacology; D019344:Lactic Acid; D008297:Male; D009206:Myocardium / Q000378:metabolism; D009638:Norepinephrine / Q000378:metabolism*; D010042:Ouabain / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D013564:Sympathetic Nervous System / Q000502:physiology*; D014649:Vas Deferens / Q000294:innervation / Q000378:metabolism*
D065098:Catechol O-Methyltransferase Inhibitors; D007773:Lactates; D019344:Lactic Acid; D010042:Ouabain; D005947:Glucose; D002118:Calcium; D003891:Desipramine; D009638:Norepinephrine