Ouabain distinguishes between nicotinic and muscarinic receptor‐mediated catecholamine secretions in perfused adrenal glands of cat

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Abstract
The effect of ouabain on catecholamine (adrenaline and noradrenaline) secretion induced by agents acting on cholinoceptors was studied in perfused cat adrenal glands. Acetylcholine (ACh) (5 × 10−7 to 10−3m), pilocarpine (10−5 to 10−3m) and nicotine (10−6 to 5 × 10−5m) caused dose‐dependent increases in catecholamine secretion. Both ACh and nicotine released more noradrenaline than adrenaline and the reverse was the case for pilocarpine. Ouabain (10−5m) enhanced catecholamine secretion induced by ACh (10−5m), pilocarpine (10−3m) and nicotine (3 × 10−6m) during perfusion with Locke solution. The ratio of adrenaline to noradrenaline was not affected by ouabain. In the absence of extracellular Ca2+, ACh and pilocarpine, but not nicotine, still caused a small increase in catecholamine secretions, which were enhanced by treatment with ouabain (10−5m) plus Ca2+ (2.2 mm) for 25 min. The effect of ouabain was much more significant on noradrenaline secretion than on adrenaline secretion. The enhanced response was blocked by atropine (10−6m) but not by hexamethonium (5 × 10−4m). Nifedipine (2 × 10−6m) inhibited the responses to pilocarpine and nicotine. The treatment with ouabain (10−5 m) reversed only the response to pilocarpine and resulted in a significant increase in the proportion of noradrenaline released. It is suggested that ouabain enhances evoked catecholamine secretions by facilitating Ca2+ entry through nicotinic receptor‐linked Ca2+ channels and by increasing the intracellular Ca2+ pool linked to muscarinic receptors.