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Plasma Norepinephrine Levels Are Influenced by Sodium Intake, Glucocorticoid Administration, and Circadian Changes in Normal Man^*

Endocrinology-Metabolism Division, UCLA School of Medicine, Sepulveda Veterans Administration Medical Center Sepulveda, California 91343; and Endocrine Sciences, Tarzana, California 91356

Address requests for reprints to: Michael L. Tuck, M.D., Sepulveda Veterans Administration Medical Center, 16111 Plummer Street, Sepulveda, California 91343.

We examined the influences of factors that may contribute to blood pressure regulation, including sodium homeostasis, ACTH, and circadian rhythm, on plasma norepinephrine (NE) levels in normal man. Basal supine NE levels and their response to 2 h of upright posture were examined in eight subjects studied after 5 days on either low (20 meq), normal (120 meq), or high (200 meq) sodium diets. Sodium depletion increased and sodium loading decreased basal supine plasma NE. Low, but not high, sodium diets had a significant effect on plasma NE responses to upright posture. However, more acute sodium loading, with isotonic saline infusion for 4 h, had no effect on plasma NE. The administration of ACTH (40 U, im, for 31 days) had no significant effect on supine and upright plasma NE. However, dexamethasone administration (0.5 mg, orally, four times daily for 3 days depressed (P 0.05) both basal NE and its response to upright posture. Noctural and daytime recumbent secretory patterns of NE and blood pressure levels were also determined at 20-min intervals in nine subjects with polygraphic monitoring to determine stages of sleep. Mean plasma NE levels were lowest at 0400–0600 h (125–150 pg/ml), rose abruptly before awakening, and reached peak concentrations at 0900 h (340 ± 27 pg/ml). All subjects had seven or more secretory peaks (NE, 25% above the mean 24-h concentration), most occurring between 0600–1800 h. Nocturnal secretion of NE was unrelated to rapid eye movement and non-rapid eye movement sleep but was correlated (r = 0.63; P 0.001) with mean arterial pressure. These findings demonstrate that several factorsmay have an important influence on the daily regulation of NE secretion. Chronic, but not acute, changes in sodium balance alter basal and postural NE secretion. The administration of glucocorticoids suppresses basal and posture-stimulated NE. Since ACTH did not alter plasma NE, this could represent a direct inhibitory effect of glucocorticoids on NE secretion. NE is released in secretory bursts and displays a circadian biorhythm that is not sleep associated but correlates with changes in mean arterial pressure. (J. Clin Endocrinol Metab 51: 1340, 1980)

^* Presented at the 61st Annual Meeting of The Endocrine Society, Anaheim, CA, 1979.

Received April 8, 1980.

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