Effect of the dihydropyridine Bay K 8644 on the release of [3H]‐noradrenaline from the rat isolated vas deferens

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Abstract
1 The effects of Bay K 8644 on the release of [3H]-noradrenaline evoked by potassium, electrical stimulation or tyramine from the rat isolated vas deferens labelled with [3H]-noradrenaline were investigated. 2 Bay K 8644 (1 μM) by itself did not affect the spontaneous release of tritium from the rat isolated vas deferens. However, it increased the calcium-dependent release of tritium elicited by both high potassium (59 mM) and electrical field stimulation. 3 The exposure of rat vas deferens to phentolamine (10 μM) increased the release of tritium induced by potassium (59 mM) and electrical field stimulation. Bay K 8644 (1 μM) failed to increase further the release of tritium elicited by both stimuli in preparations previously treated with phentolamine (10 μM). 4 The calcium-independent release of [3H]-noradrenaline evoked by tyramine (10 μM) was not affected by Bay K 8644 (1 μM). 5 The results of our study support the view that α2-adrenoceptors modulate noradrenaline release by restricting calcium influx into sympathetic nerve terminals through voltage-dependent channels.