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Release of noradrenaline by 1 pulse modulation of such release by alpha adrenoceptor antagonists and uptake blockers



Release of noradrenaline by 1 pulse modulation of such release by alpha adrenoceptor antagonists and uptake blockers



Naunyn-Schmiedeberg's Archives of Pharmacology 317(4): 302-309



A simple method for studying sympathetic neurosecretion in the mammalian heart in response to nerve stimulation was introduced. Whether or not presynaptic .alpha.-adrenoceptors and high affinity uptake mechanism of cardiac sympathetic nerves play some role in the regulation of noradrenaline [norepinephrine, NE] release evoked by 1 pulse was determined. NE overflow induced by a train of impulses (1 Hz for 180 s) in the isolated perfused heart of the guinea pig was enhanced in a dose-dependent manner by phentolamine or phenoxybenzamine, and the extent of enhancement was comparable. NE overflow was not altered upon excitation of sympathetic nerve by 1 pulse. Addition of phentolamine, phenoxybenzamine, yohimbine or uptake blockers (cocaine, desipramine and corticosterone) to the perfusion medium did not modify the overflow. NE overflow induced by 1 pulse was enhanced by K-channel blockers (4-aminopyridine or tetraethylammonium, TEA). 3H-NE overflow induced by 1 shock in the presence of TEA was further enhanced .apprx. 2-fold by .alpha.-adrenoceptor antagonists. At 1 Hz, these agents enhanced the overflow also 2-fold. The overflow of 3H-NE induced by 1 shock or 1 Hz (in the presence of TEA) was enhanced > 2-fold by desipramine. The release of sympathetic transmitter upon 1 shock is under the control of presynaptic .alpha.-adrenergic receptors. NE released in the very early part of the exocytosis could interfere with the remaining part of the same release process by modulating the availability of Ca. The neuronal uptake process plays an important role in removing NE released even after 1 pulse.

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Accession: 006306169

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