Choline administration to the rat increases urinary catecholamines

Summary

Previous studies have shown that choline administration accelerates the synthesis of acetylcholine (ACh) in rats and raises ACh levels in brain, adrenal medulla, and other tissues receiving a cholinergic innervation. After 24 hours, this precursor-induced elevation in ACh levels causes tyrosine hydroxylase activity to increase, unless the adrenals have been previously denervated. We now report that oral choline administration also increases urinary epinephrine levels, probably by enhancing the release of the catecholamine from the adrenal gland. For four consecutive 4-day periods, male Sprague-Dawley rats received (1) no treatment, (2) water, (3) choline (20 mmoles/kg), and (4) water, and excreted 157, 200, 646, and 267 ng of epinephrine per 24-hour period, respectively. Urinary norepinephrine levels also increased on days that the animals received choline. Choline failed to increase urinary epinephrine levels among rats previously subjected to bilateral adrenal denervation; in contrast, nicotine, a direct-acting cholinergic agonist, continued to elicit this increase. Thus, choline administration apparently potentiates the increase in urinary epinephrine produced by treatments that accelerate the flow of impulses along the splanchnic nerves. These data provide additional support for the hypothesis that choline administration, by increasing presynaptic ACh levels, enhances cholinergic transmission at preganglionic synapses of the sympathetic nervous system.