17b-estradiol modifies nitric oxide-sensitive guanylyl cyclase expression and down-regulates its activity in rat anterior pituitary gland.

JIMENA P. CABILLA, MARÍA DEL CARMEN DÍAZ, LETICIA I. MACHIAVELLI, ARIEL H. B. POLIANDRI, ALNILAN F. QUINTEROS, MERCEDES LASAGA AND BEATRIZ H. DUVILANSKI.

ENDOCRINOLOGY

THE ENDOCRINE SOCIETY

Año: 2006 vol. 147 p. 4311 - 4318

0013-7227

Previous studies showed that 17
-estradiol (17
-E2) regulates the nitric oxide (NO)/soluble guanylyl cyclase (sGC)/cGMP pathway in many tissues. Evidence from our laboratory indicates that 17
-E2 disrupts the inhibitory effect of NO on prolactin release, decreasingsGCactivity and affecting thecGMP pathway in anterior pituitary gland of adult ovariectomized and estrogenized rats. To ascertain the mechanisms by which 17
-E2 affects sGC activity, we investigated the in vivo and in vitro effects of 17
-E2 on sGC protein and mRNA expression in anterior pituitary gland from immature female rats. In the present work, we showed that 17
-E2 acute treatment exerted opposite effects on the two sGC subunits, increasing 1 and decreasing
1 subunit protein and mRNA expression. This action on sGC protein expression was maximal 6–9 h after 17
-E2 administration. 17
-E2 also caused the same effect on mRNAexpression at earlier times. Concomitantly, 17
-E2 dramatically decreased sGC activity 6 and 9 h after injection.
-estradiol (17
-E2) regulates the nitric oxide (NO)/soluble guanylyl cyclase (sGC)/cGMP pathway in many tissues. Evidence from our laboratory indicates that 17
-E2 disrupts the inhibitory effect of NO on prolactin release, decreasingsGCactivity and affecting thecGMP pathway in anterior pituitary gland of adult ovariectomized and estrogenized rats. To ascertain the mechanisms by which 17
-E2 affects sGC activity, we investigated the in vivo and in vitro effects of 17
-E2 on sGC protein and mRNA expression in anterior pituitary gland from immature female rats. In the present work, we showed that 17
-E2 acute treatment exerted opposite effects on the two sGC subunits, increasing 1 and decreasing
1 subunit protein and mRNA expression. This action on sGC protein expression was maximal 6–9 h after 17
-E2 administration. 17
-E2 also caused the same effect on mRNAexpression at earlier times. Concomitantly, 17
-E2 dramatically decreased sGC activity 6 and 9 h after injection. These effects were specific of 17
-E2, because they were not observed with the administration of other steroids such as progesterone and 17-estradiol. This inhibitory action of 17
-E2 on sGC also required the activation of estrogen receptor (ER), because treatment with the pure ER antagonist ICI 182,780 completely blocked 17
-E2 action. 17
-E2 acute treatment caused the same effects on pituitary cells in culture. These results suggest that 17
-E2 exerts an acute inhibitory effect on sGC in anterior pituitary gland by down-regulating sGC
1 subunit and sGC activity in a specific, ER-dependent manner. (Endocrinology 147: 4311–4318, 2006)-