The interaction between extracellular catecholamines and catecholamine secretion from chromaffin cells was assessed in rainbow trout (Oncorhynchus mykiss) using an in situ saline-perfused posterior cardinal vein preparation. This was accomplished by comparing the effects of adrenergic receptor agonists and antagonists on stimulus-evoked secretion. An acute bolus injection or extended perfusion with saline containing high levels of either noradrenaline or adrenaline did not affect the baseline secretion of catecholamines. However, catecholamine secretion in response to a bolus injection of the general cholinergic receptor agonist carbachol or electrical stimulation of the nerves innervating the chromaffin cells was abolished or reduced respectively, in preparations perfused with saline containing either catecholamine. To characterize the catecholaminergic inhibition of catecholamine release, secretion in response to carbachol and electrical stimulation was compared in preparations perfused with the adrenergic receptor agonists dobutamine (beta(1)), salbutamol (beta(2)), phenylephrine (alpha(1)) or clonidine (alpha(2)). Prior treatment with dobutamine or phenylephrine was without effect on baseline catecholamine secretion or stimulus-evoked secretion. In contrast, pre-treatment with salbutamol significantly inhibited catecholamine secretion in response to carbachol or electrical stimulation. Pre-treatment with clonidine did not affect carbachol-evoked secretion but did reduce catecholamine secretion during electrical stimulation. The significance of this adrenergic mechanism of regulating stimulus-evoked catecholamine secretion was further established using the adrenergic receptor antagonists nadolol (beta) or phentolamine (alpha). Catecholamine secretion in response to cholinergic stimulation was significantly enhanced in preparations perfused with saline containing nadolol. Furthermore, pre-treatment with phentolamine significantly enhanced adrenaline secretion in response to neuronal stimulation. These results suggest that the mechanisms of adrenergic inhibition of catecholamine secretion from trout chromaffin cells include activation of chromaffin cell membrane beta(2)-receptors and presynaptic alpha(2)-adrenergic receptors.
Beta-2 Adrenergic Receptor Agonists Enhance AChR Clustering in C2C12 Myotubes: Implications for Therapy of Myasthenic Disorders