Effects of prolonged adrenaline infusion and of mental stress on plasma minerals and parathyroid hormone
- 1 January 1990
- journal article
- research article
- Published by Wiley in Clinical Physiology and Functional Imaging
- Vol. 10 (1), 37-53
- https://doi.org/10.1111/j.1475-097x.1990.tb00082.x
Abstract
The role of the sympatho-adrenal system for the secretion of PTH in humans is not established. Previous studies on the effects of adrenaline on plasma mineral homeostasis have focused on injections or short-term infusions of adrenaline, and conflicting results concerning calcium and parathyroid hormone (PTH) responses have been reported. We therefore infused adrenaline or placebo continuously for 3 h to 10 healthy volunteers and studied several plasma minerals, as well as PTH levels. Venous plasma adrenaline concentrations increased to the upper physiological range (5 nmol l-1) during adrenaline infusion. Another nine volunteers were exposed for 25 min to mental stress (a colour word conflict test; CWT), which causes marked circulatory changes and raises plasma catecholamine concentrations. Plasma ionized and total calcium, and magnesium concentrations were slowly and gradually reduced during infusion of adrenaline, but there was only a small increase in PTH. Plasma potassium was decreased by adrenaline within 30 min and thereafter did not change further during infusion. There was a marked but transient increase in the plasma free fatty acids concentrations, which were not related to the reduction of the calcium or magnesium levels. The adrenaline-induced decrements in calcium, magnesium and potassium, and increases in heart rates persisted 30 min after the infusion, despite a rapid decrease in plasma adrenaline concentrations within 5 min of termination of the infusion. Plasma phosphate concentrations were lowered during the first 90 min of adrenaline infusion, but after 3 h they had returned to baseline despite continued infusion. CWT induced small increments of the plasma ionized calcium and PTH concentrations. Plasma potassium levels were raised despite increases in plasma adrenaline at the beginning of the stress test, while phosphate values were reduced at the end of the test. Thus, long-lasting elevations of circulating adrenaline lower plasma ionized and calcium, phosphate, magnesium and potassium, but the time courses for these changes differed markedly. Despite the reduction of plasma ionized calcium there was only little increase in PTH and thus no indication that sustained elevations of circulating adrenaline stimulates the secretion of PTH in vivo in humans. Responses to acute mental stress and adrenaline infusion differed qualitatively, indicating that adrenaline responses to stress are of minor importance in this respect.Keywords
This publication has 36 references indexed in Scilit:
- Stimulation of parathyroid hormone secretion by EDTA infusion – a test for the differential diagnosis of hypercalcaemiaActa Endocrinologica, 1986
- Changes in Parathyroid Hormone and Calcium Levels after Superior Cervical Ganglionectomy of RatsNeuroendocrinology, 1985
- Hypokalemia from Beta2-Receptor Stimulation by Circulating EpinephrineNew England Journal of Medicine, 1983
- Measurements of plasma norepinephrine concentrations in human primary hypertension. A word of caution on their applicability for assessing neurogenic contributions.Hypertension, 1983
- Adrenergic control of Na+‐K+‐homoeostasisActa Medica Scandinavica, 1983
- Serum phosphate shift in acute myocardial infarctionAmerican Heart Journal, 1982
- Ionized Calcium and the in vivo Response of Normal and Hyperplastic Parathyroid Glands to Beta-Adrenergic AgentsNephron, 1982
- Serial plasma catecholamine response early in the course of clinical acute myocardial infarction: Relationship to infarct extent and mortalityAmerican Heart Journal, 1981
- Physiology and Pathophysiology of the Human Sympathoadrenal Neuroendocrine SystemNew England Journal of Medicine, 1980
- Determination of plasma catecholamines by high performance liquid chromatography with electrochemical detection: Comparison with a radioenzymatic methodLife Sciences, 1979