Potassium deficiency produced by feeding mice a low
potassium diet caused a marked decrease in plasma and testicular
testosterone concentrations and a concomitant fall in the weight of seminal vesicles and in renal
ornithine decarboxylase activity. All of these parameters were rapidly restored when
potassium supply was normalized. Immunocytochemical analysis of gonadotropes and plasma LH values suggested that the pulsatile liberation of LH by the pituitary was impaired in the
potassium-deficient male mice. Because the synthesis of
testosterone in the
potassium-deficient mice was stimulated by exogenous LH, hCG, or
GnRH, one can conclude that alteration of the transcellular
potassium gradient could affect the regulation of the hypothalamo-hypophyseal-testicular axis by affecting the pulsatile release of
GnRH. Our results showing that the stimulation of LH secretion after
castration was similar in control and
potassium-deficient male mice suggest that a testicular factor(s) different from
testosterone could be implicated in the abnormal regulation of LH secretion in
potassium-deficient mice. We conclude that plasma
potassium concentration is an important factor in the regulation of
gonadotropin secretion and testicular functions.