Uptake and release of catecholamines in sympathetic nerve fibres in the spleen of the cod, Gadus morhua.

Abstract

The effects of drugs known from mammalian experiments to interfere with uptake and release of adrenergic transmitters in the sympathetic nerve terminals have been investigated on perfused spleen and isolated spleen strips from the cod. Cocaine and desipramine inhibit the accumulation of 3H-noradrenaline in the perfused spleen, probably by interfering with uptake mechanisms. Both drugs also shift to the left the dose-response curves for noradrenaline and adrenaline on isolated strips, cocaine being most potent. The maximal contraction force of isolated strips also increases after cocaine when noradrenaline is the agonist, but not when methacholine is used or on chronically denervated strips. This effect of cocaine is therefore not due to a general postsynaptic effect. Tyramine and amphetamine both release stored 3H-noradrenaline from the perfused spleen, and tyramine also contracted the spleen strips. In contrast to the situation in mammals, the dose-response curve for tyramine is not affected by cocaine, and tyramine (up to 10(-3) M) present in the bath does not potentiate the dose-response curve for noradrenaline on isolated strips. Different uptake mechanisms for tyramine and noradrenaline into the nerve terminal are therefore suggested for the cod sympathetic fibres. The alpha-adrenoceptor blocking agent phentolamine produces an increase in overflow of label during nerve stimulation at 5Hz in the perfused spleen preloaded with 3H-noradrenaline. An alpha-adrenoceptor-mediated control of the release of catecholamines, similar to that in mammals, appears to be present in the cod.