Effects of nanomolar to submillimolar carteolol, a non-selective β-antagonist, on the evoked release at 1 Hz and the spontaneous release in the absence and presence of uptake
1 and uptake
2 blockers were studied in pulmonary arteries, isolated from guinea pigs, and then preloaded with [
3H] noradrenaline. dl-Carteolol at 10
-8, 10
-7 and 10
-6 M applied at the increasing concentrations inhibited the evoked [
3H]-release in untreated arteries and in desipramine and corticosterone-treated arteries. The spontaneous [
3H]-release slightly but significantly increased or tended to increase in untreated arteries. dl-Carteolol at 10
-5 and 10
-4 M clearly and concentration-dependently increased the spontaneous [
3H]-release in untreated and cocaine-treated arteries. This increase was markedly inhibited by further pretreatment with normetanephrine. The evoked [
3H]-release was not altered by dl-carteolol at 10
-5 M, but increased at 10
-4 M. This increase was not modified by cocaine and by cocaine and normetanephrine. d-Carteolol at 10
-5 and 10
-4 M produced effects similar to those of dl-carteolol. Nanomolar to micromolar dl-carteolol inhibits the evoked [
3H]-release, which supports our previous conclusion that this inhibition is due to blockade of tonically functioning presynaptic β
2-adrenoceptors. Carteolol at the higher concentrations seems to become a substrate for an uptake
2 mechanism and to produce an unknown sympathomimetic activity in guinea pig pulmonary arteries.
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