Hypokalemia alters sex hormone and gonadotropin levels: evidence that FSH may be required for luteinization

• Published in: American journal of physiology: endocrinology and metabolism 1998-12, Vol.275 (6), p.E1037-E1045
• Main Authors: Tejada, Francisco, Cremades, Asuncion, Aviles, Manuel, Castells, Maria T, Penafiel, Rafael
• Format: Article
• Language: English
• ISSN: 0193-1849; 1522-1555
• DOI: 10.1152/ajpendo.1998.275.6.E1037

Departments of 1  Pharmacology, 2  Cell Biology, and 3  Biochemistry and Molecular Biology, Faculty of Medicine, University of Murcia, 30100 Murcia, Spain Hypokalemia produced different effects on steroid sex hormone concentrations in plasma and ovary in the mouse. Estradiol levels were slightly increased, whereas circulating progesterone was markedly decreased in all estrous periods. The preovulatory surge of gonadotropins and the secondary surge of follicle-stimulating hormone (FSH) at estrus were also decreased, but basal levels of both gonadotropins were unaffected. Supplementation with luteinizing hormone (LH), FSH, or gonadotropin-releasing hormone (GnRH) at proestrus rapidly normalized plasma and ovarian progesterone levels at this stage of the estrous cycle. Plasma progesterone levels at diestrus were restored only by combined treatment, at the periovulatory stage, with LH and FSH or GnRH but not by LH or FSH alone. The results demonstrate a lack of steroidogenic activity in the corpus luteum of the potassium-deficient mice and, furthermore, that FSH plays an important role in luteinization in the hypokalemic mice. We conclude that alteration of the transcellular potassium gradient may affect the regulation of the periovulatory surge of gonadotropins and progesterone secretion, probably by altering the release of GnRH from the hypothalamus. In addition, the results suggest that FSH may play a certain role as a luteotropic hormone in mice. potassium; corpus luteum; gonadotropin-releasing hormone; mice