The outward transport of axoplasmic noradrenaline induced by a rise of the sodium concentration in the adrenergic nerve endings of the rat vas deferens.
The adrenergic nerve endings of the rat vas deferens were loaded with 3H-(-)-noradrenaline; COMT was inhibited by the presence of 10 mumol/l U-0521, and all experiments were carried out with calcium-free solution. After 100 min of wash-out a neuronal efflux of tritium was obtained which remained constant with time (when expressed as fractional rate of loss; FRL); it contained more DOPEG than noradrenaline. The in vitro administration of reserpine-like drugs (reserpine and Ro 4-1284) increased the FRL of tritium, presumably because of an increase in the leakage of noradrenaline from storage vesicles; the efflux of DOPEG increased more than that of noradrenaline, and the ratio NA/DOPEG declined. Inhibition of the membrane ATPase (by omission of potassium from the medium or by the presence of 3 mmol/l ouabain) increased the FRL of tritium, presumably because of an increase in the net leakage of noradrenaline from the storage vesicles (as a consequence of the fall in the concentration of free axoplasmic noradrenaline; see below). Veratridine also increased the FRL of tritium, partly because of its known reserpine-like effect (Bönisch et al. 1983); in the presence of 1 mumol/l veratridine, the efflux of DOPEG increased. Irrespective of the presence or absence of reserpine or Ro 4-1284, inhibition of the membrane ATPase or the presence of veratridine (agents or procedures which increase the axoplasmic sodium concentration) always resulted in a brisk increase of the efflux of noradrenaline that was accompanied by a simultaneous decrease in the efflux of DOPEG (see above for one exception).(ABSTRACT TRUNCATED AT 250 WORDS)
D012369:2H-Benzo(a)quinolizin-2-ol, 2-Ethyl-1,3,4,6,7,11b-hexahydro-3-isobutyl-9,10-dimethoxy- / Q000494:pharmacology; D000251:Adenosine Triphosphatases / Q000037:antagonists & inhibitors; D000320:Adrenergic Fibers / Q000378:metabolism*; D000818:Animals; D001370:Axonal Transport / Q000187:drug effects; D003000:Clonidine / Q000494:pharmacology; D066298:In Vitro Techniques; D007700:Kinetics; D008297:Male; D008734:Methoxyhydroxyphenylglycol / Q000031:analogs & derivatives / Q000378:metabolism; D009411:Nerve Endings / Q000378:metabolism*; D009638:Norepinephrine / Q000378:metabolism*; D010042:Ouabain / Q000494:pharmacology; D010646:Phentolamine / Q000494:pharmacology; D011188:Potassium / Q000378:metabolism; D051381:Rats; D012110:Reserpine / Q000494:pharmacology; D012964:Sodium / Q000378:metabolism*; D014649:Vas Deferens / Q000294:innervation*; D014701:Veratridine / Q000494:pharmacology
D012369:2H-Benzo(a)quinolizin-2-ol, 2-Ethyl-1,3,4,6,7,11b-hexahydro-3-isobutyl-9,10-dimethoxy-; D008734:Methoxyhydroxyphenylglycol; D010042:Ouabain; D014701:Veratridine; D012110:Reserpine; D012964:Sodium; D000251:Adenosine Triphosphatases; D003000:Clonidine; D011188:Potassium; C010117:3,4-dihydroxyphenylglycol; D009638:Norepinephrine; D010646:Phentolamine