No abstract

No abstract

A study of the mechanism of release of [3H]‐noradrenaline ([3H]‐NA) by nicotine from isolated vas deferens of the rat was made using incubation media of different ionic composition. Nicotine (20 μg/ml)‐induced release of [3H]‐NA was significantly potentiated in K+‐free Krebs solution as compared to that in normal Krebs‐Ringer solution. Nicotine‐induced release of [3H]‐NA was significantly reduced in Na+‐deficient Krebs solution (containing only 11 mM Na+) and was abolished in Na+‐free Krebs solution. In totally depolarized tissues, nicotine failed to cause an outflow of [3H]‐NA but Ca2+ (5 mM) did so. Nicotine required the presence of Ca2+ in the incubation medium to cause release of [3H]‐NA from adrenergic nerve terminals, the magnitude of release being dependent upon the concentration of Ca2+. Nicotine‐induced release of [3H]‐NA was demonstrated in high Ca2+, Na+‐free Krebs solution in which all Na+ had been replaced with Ca2+. It is concluded that nicotine increases the membrane permeability to both Na+ and Ca2+. It is also suggested that the increase in permeability to Ca2+ alone is not sufficient but a local depolarizing action of nicotine is necessary to cause release of noradrenaline from adrenergic nerve endings.

No abstract

No abstract