Acute stimulation of intestinal cell calcium influx induced by 17ß estradiol via cAMP messengers system.

PICOTTO G,; MASSHEIMER VIRGINIA; BOLAND R

MOLECULAR AND CELLULAR ENDOCRINOLOGY.

ELSEVIER IRELAND LTD

Año: 1996 vol. 119 p. 129 - 134

0303-7207

Recent studies have provided evidence for nuclear estrogen receptor-mediated calcium transport in intestinal mucosal cells. The possibility that, in addition, estrogens directly stimulate intestinal Ca2+ fluxes through second-messenger pathways was investigated. Exposure of enterocytes isolated from female rat duodenum to low physiological levels of 17â-estradiol (10−11, 10−10 and 10−8 M) rapidly (1–10 min) increased (50–170%) cell 45Ca2+ influx. 17á-Estradiol, dihydrotestosterone and progesterone were devoid of activity, suggesting specificity of the estrogen effect. Maximum responses induced by 17â-estradiol (5 min at 10−10 M) could be abolished to a great extent (84%) by pretreating the cells with verapamil (10 ìM) and nitrendipine (1 ìM), involving the activation of voltage-dependent Ca2+ channels in the fast increase of rat duodenal calcium uptake by the hormone. Evidence was obtained indicating that the acute estrogen stimulation of enterocyte Ca2+ influx is mediated by the cyclic AMP/PKA pathway. 17â-Estradiol rapidly increased cAMP content of rat duodenal cells in parallel to the changes in Ca2+ uptake. In addition, forskolin, dibutyryl cAMP and Sp-cAMPS mimicked and Rp-cAMPS suppressed the prompt 17â-estradiol-induced stimulation of Ca2+ influx. These results are consistent with a direct action of estrogens in the enterocyte, presumably a non-genomic one, initiated on the cell surface and resulting in rapid activation of the cAMP pathway and Ca2+ channels, which may be relevant for regulation of intestinal calcium transport.