STIMULATION OF PRESYNAPTIC β-ADRENOCEPTORS ENHANCES [3H]-N0RADRENALINE RELEASE DURING NERVE STIMULATION IN THE PERFUSED CAT SPLEEN

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Abstract
1 The effects of isoprenaline, propranolol and phosphodiesterase inhibitors on 3H-transmitter overflow elicited by low frequency nerve stimulation were determined in the isolated perfused spleen of the cat. 2 (-)-Isoprenaline (0.14, 1.4, and 14 nm) produced a concentration-dependent increase in [3H]-transmitter overflow evoked by nerve stimulation at 1 Hz and was more effective at 1 Hz than at 2 hertz. 3 A concentration of propranolol (0.1 μm), devoid of neurone blocking activity, blocked this effect of (—)-isoprenaline. These results are compatible with the presence of β-adrenoceptors in the noradrenergic nerve endings of the cat spleen. 4 (-l-)-Isoprenaline (140 nm) failed to increase the release of radioactivity induced by nerve stimulation, indicating that the β-adrenoceptor mediating the facilitation of transmitter release was stereo-specific. 5 The increase in 3H-transmitter overflow induced by nerve stimulation during exposure to the phosphodiesterase inhibitor, papaverine (27 μm) was more pronounced than that obtained in the presence of 3-isobutyl-l-methyl xanthine (IBMX) 0.5 mm. The facilitation in transmitter release induced by papaverine was not correlated with the granular effect produced by this drug. 6 In the presence of papaverine, the concentration-effect curve for (—)-isoprenaline on transmitter release was shifted to the left and its maximum was increased. In addition, propranolol significantly reduced the enhancement in noradrenaline release obtained by exposure to papaverine under conditions in which the granular effect produced by the phosphodiesterase inhibitor was even greater than in the absence of the P-blocker. 7 It is concluded that activation of presynaptic p-adrenoceptors in the perfused cat spleen leads to an enhancement in transmitter release which appears to be linked to an increase in cyclic adenosine 3′, 5′-monophosphate levels in noradrenergic nerve endings.

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