Abstract
The effect of Bay K 8644 (a dihydropyridine Ca2+-channel activator), was examined on spontaneous and stimulus-evoked release of tritium from isolated rat atria prelabelled with [3H]-noradrenaline. Bay K8644 (3μmol/l) significantly increased atrial rate from 206±7 to 259±9 beats·min-1 (P<0.05) and also tritium outflow (expressed as fractional rate of loss in min- × 103) from 6.49±0.35 to 8.61±0.74 (P<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.
Original language | English (US) |
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Pages (from-to) | 603-608 |
Number of pages | 6 |
Journal | Naunyn-Schmiedeberg's Archives of Pharmacology |
Volume | 343 |
Issue number | 6 |
DOIs | |
State | Published - Jun 1991 |
Externally published | Yes |
Keywords
- Adrenergic nerve endings
- Bay K 8644
- Rat atria
- Tritium efflux
- [H]-noradrenaline
ASJC Scopus subject areas
- Pharmacology