Taizo Suzuki

Neuronal norepinephrine as mediator for ouabain-induced smooth muscle contraction.

With some latency, ouabain (10(-6)--10(-5) M) induced a long-lasting contractile response of the isolated vas deferens of the guinea-pig. The ouabain-induced contraction was potentiated by pretreatment with tropolone, whereas it was prevented by pretreatment with cocaine, bretylium, reserpine or phentolamine. The response was unaffected byatropine, methysergide and tetrodotoxin. Ouabain, perfused into the isolated tissue, enhanced dose-dependently the release of norepinephrine into the medium. However, this enhancement of norepinephrine release was prevented by reserpine or by removal of Ca from the medium. These findings support the hypothesis that the ouabain-induced contraction of vas deferens might be due to norepinephrine released from the adrenergic nerve ending granules through a Ca2+-dependent process.

Effects of calcium-removal and sodium-potassium adenosine triphosphatase inhibition on the release of epinephrine from the extraneuronal site

Abstract Releases of unchanged epinephrine from the extraneuronal site of the isolated guinea-pig vas deferens were fluorimetrically determined by direct trihydroxyindole reaction at two different pH. The spontaneous release of the amine from the normal preparation preloaded with 3 x 10−5 M epinephrine was significantly enhanced by inhibitions of Na-K ATPase or by Ca-removal. After epinephrine loading, the release of the amine from the preparation pretreated with pargyline and pyrogallol or from the denervated preparation was also enhanced by the both procedures. These enhanced releases of the amine were prevented by pretreatment of clonidine, Uptake 2 inhibitor, preceded the epinephrine loading. From these results, it was suspected that the retention or the release of the extraneuronal catecholamine in the vas deferens might be partly modified through the alteration of the Na-K ATPase activity and Ca concentration of the cell membrane.