Abstract
The effect of Bay K 8644 (a dihydropyridine Ca(2+)-channel activator), was examined on spontaneous and stimulus-evoked release of tritium from isolated rat atria prelabelled with [3H]-noradrenaline. Bay K 8644 (3 mumol/l) significantly increased atrial rate from 206 +/- 7 to 259 +/- 9 beats.min-1 (P less than 0.05) and also tritium outflow (expressed as fractional rate of loss in min-1 x 10(3)) from 6.49 +/- 0.35 to 8.61 +/- 0.74 (P less than 0.05). Neither the maximal rate nor the overflow of tritium induced by stimulation of sympathetic nerve terminals was changed by the compound. The increase in basal tritium outflow produced by Bay K 8644 was calcium-dependent. However, it could not be antagonized by nitrendipine. The overflow of tritium induced by Bay K 8644 consisted mainly of 3,4-dihydroxyphenylglycol ([3H]-DOPEG), indicating that the compound produces a leakage from the storage vesicles of sympathetic nerve terminals of the isolated rat atria.
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