Inhibition of adrenomedullary catecholamine release by propranolol isomers and clonidine involving mechanisms unrelated to adrenoceptors.

摘要: 1 Transmural electrical stimulation (10 Hz, 40 V, ms for 60s) increased total catecholamine secretion from perfused cat adrenal glands; this response was enhanced by neostigmine and inhibited mecamylamine, suggesting that release of acetylcholine splanchnic nerve terminals stimulating nicotinic receptors enhancing secretion. 2 Isoprenaline, (-)-propranolol (+)-propranolol (10(-7)-10(-5)M) the electrically-evoked secretory 40-70%; similar reductions were obtained with clonidine yohimbine. Neither, nor K-evoked adrenals; in contrast, nimodipine potently it (IC50 = 24 nM). 3 Either, racemic propranolol or (+)- (-)-isomers (1-10 microM) equally [3H]-noradrenaline evoked nicotine cultured bovine chromaffin cells; 50% yohimbine isoprenaline did not affect it. 4 The results indicate adrenomedullary is modulated alpha- beta-adrenoceptors suggest may inhibit blocking ion fluxes through receptor ionophore. Clonidine same mechanism, and/or interfering some intracellular event mechanism.