The release of acetylcholine and of catecholamine from the cat's adrenal gland

The cat's adrenal gland was perfused in situ with Krebs solution containing eserine; the amount of acetylcholine and of catecholamine released was measured. Splanchnic nerve stimulation (5 Hz for 2 min) increased the release of acetylcholine and catecholamine; the molar ratio of evoked release of catecholamine to acetylcholine was122 ± 8. It is suggested that this amplification is achieved because a chromaffin cell granule contains more mediator than does the acetylcholine quantum that releases it. The release per impulse of catecholamine during splanchnic nerve stimulation at 30 Hz was less than that released by stimulation at 1 or 5 Hz. This depression is attributed to a presynaptic failure, because the release of acetylcholine was similarly frequency dependent. The release of catecholamine was linearly related to the release of acetylcholine over the range tested, indicating that the input-output relationship at the splanchnic-adrenal medullary junction is linear. During continuous stimulation of the splanchnic nerve (5 Hz), catecholamine release declined to a level that was32 ±2% of the initial output. This fatigue is attributed primarily to a postsynaptic depression, because the release of acetylcholine was maintained at71±6% of its initial level. The presence of eserine in the perfusate was necessary for the release of acetylcholine to be detected, but in the presence of eserine catecholamine release was90±10% that in the drug's absence. It is concluded that released acetylcholine is hydrolysed at some distance from its site of release and action. Glands perfused with raised K + released acetylcholine and catecholamine. During a 10 min exposure to K +, catecholamine release was less well maintained than was acetylcholine release. It is suggested that calcium channels on adrenal cells desensitize more readily than those on cholinergic nerve terminals. Muscarine or nicotine released catecholamine but not acetylcholine; acetylcholine antagonists depressed evoked catecholamine release but did not alter acetylcholine release. These findings are interpreted to indicate that compounds secreted from the adrenal medulla have no physiologically important feed-back effects on cholinergic nerve terminals.