Hormonal secretory mechanisms are influenced positively or negatively by magnesium, the effect depending on its concentration. The submitted study is concerned with the effect of acute hypermagnesemia induced by intravenous infusion of 6 g MgSO4 on quiescent and LHRH-induced secretion of FSH, LH, prolactin and testosterone; on the levels of intact parathyroid hormone; and on other hormonal and mineral indicators in 10 healthy male subjects. Gonadotropin secretion was not altered by hypermagnesemia. Quiescent testosterone levels decreased moderately (p<0.01), and the secretory kinetics of the hormone slightly changed. Parathyroid hormone levels markedly dropped in the 60th minute of hypermagnesemia duration (p < 0.01), the drop depending on the initial values of the hormone prior to the administration of magnesium (r = 0,923, p < 0.01). Although in hypermagnesemia no correlations between the levels of parathyroid hormone and those of magnesium, calcium and phosphorus could be found, in normomagnesemia significant correlations were confirmed between the levels of parathyroid hormone and magnesemia (r=-0.8068, p< 0.05), and the levels of parathyroid hormone and calcemia (r = -0.9451, p < 0.01). In hypermagnesemia there were no alterations in the levels of the plasma prolactin, cortisol or catecholamines, nor was there any alteration in the rate at which catecholamines were excreted in urine. In conclusion, magnesium in supraphysiologic concentrations does not significantly change the function of the adenohypophyseal-gonadal axis or other hormonal indicators studied. The slight decline of quiescent testosterone levels does not seem to have any clinical significance, although this must be verified by further studies. The ''calcium-like'' effect of magnesium on the secretion of parathyroid hormone is proof that a biologically significant magnesium level has been attained.