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Influence of intravenous Mg++ solutions on renal excretion of potassium, sodium, calcium, chloride, intraleukocytic potassium and peripheral vascular resistance: a metabolic and hemodynamic study in normal volunteers.

In an open randomized crossover trial 8 healthy male volunteers received an intravenous infusion of potassium chloride, potassium/magnesium chloride, potassium-(D,L)-aspartate, and potassium/magnesium-(D,L)-aspartate. Equimolar amounts of potassium (27.75 mmol) and magnesium (13.9 mmol) were given in a 500-ml volume during 24 h. During two 9-day periods subjects were maintained on a constant diet with a daily intake of 80 mmol potassium and 60 mmol magnesium. Infusions were administered on day 5 and 7 of each period. Serum and urine electrolyte concentrations as well as intraleukocyte potassium were measured before, during, and after the tests; cardiac output and systemic vascular resistance were determined by impedance cardiography. Potassium and magnesium containing solutions did not influence renal elimination of potassium, and also the circadian rhythm of potassium excretion did not show any change. The elimination of sodium, calcium, potassium, and chloride rose significantly over the corresponding control values during magnesium infusions, but not when potassium salts were given. The increase of calcium excretion after Mg++ is most probably due to suppression of parathyroid hormone. Intraleukocyte potassium was not affected significantly by the various infusions, indicating that intracellular compartments are completely filled. There was no evidence that the anion (D,L-aspartate or chloride) had a significant effect on all measured variables. Mean arterial blood pressure and peripheral vascular resistance were not altered significantly during the infusions.

Adult↗

Effects of prolonged infusions of potassium chloride, adrenocorticotrophin or angiotensin II upon serum aldosterone concentration and the conversion of corticosterone to aldosterone in rats.

The temporal relation between alterations in serum aldosterone and in the conversion of labelled corticosterone to aldosterone by incubated adrenal tissue was studied in conscious rats receiving long-term infusions of KCl, ACTH or angiotensin II. When potassium-deficient rats were given KCl, a marked increase in serum aldosterone was observed only after 12 h, i.e. at a time when the conversion of corticosterone to aldosterone had become normal. After 24 h of ACTH infusion into sodium- and potassium-replete rats the serum aldosterone was markedly elevated, whereas the conversion of corticosterone to aldosterone was significantly decreased. After 48 h of continued ACTH infusion the serum aldosterone returned to normal and there was a further decrease in the conversion rate. A 24-h angiotensin II infusion into sodium- and potassium-replete rats induced significant increases in both the serum aldosterone and the conversion. After 48 h of continued angiotensin infusion the serum aldosterone returned to normal while the conversion and the blood pressure remained elevated. These results indicate that the activity of the enzymes involved in the final steps of aldosterone biosynthesis may become rate-limiting for the secretion of aldosterone during potassium deficiency and during prolonged ACTH treatment. On the other hand, the observed transiency of aldosterone stimulation by exogenous angiotensin II was not due to a suppression of the final steps of aldosterone biosynthesis and remains unexplained.

Adrenocorticotropic Hormone↗