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17ß-Estradiol Modifies Nitric Oxide-Sensitive Guanylyl Cyclase Expression and Down-Regulates Its Activity in Rat Anterior Pituitary Gland

Departamento de Química Biológica (J.P.C., M.d.C.D., L.I.M., A.H.P., F.A.Q., B.H.D.), Instituto de Química y Fisico Química Biológicas, Facultad de Farmacia y Bioquímica, and Centro de Investigaciones en Reproducción (M.L.), Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires C1113AAD, Argentina

Address all correspondence and requests for reprints to: Beatriz H. Duvilanski, Ph.D., Departamento de Química Biológica, Instituto de Química y Fisico Química Biológicas, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Junín 956, Buenos Aires (C1113AAD), Argentina. E-mail: neuroend{at}ffyb.uba.ar.

Previous studies showed that 17ß-estradiol (17ß-E2) regulates the nitric oxide (NO)/soluble guanylyl cyclase (sGC)/cGMP pathway in many tissues. Evidence from our laboratory indicates that 17ß-E2 disrupts the inhibitory effect of NO on prolactin release, decreasing sGC activity and affecting the cGMP pathway in anterior pituitary gland of adult ovariectomized and estrogenized rats. To ascertain the mechanisms by which 17ß-E2 affects sGC activity, we investigated the in vivo and in vitro effects of 17ß-E2 on sGC protein and mRNA expression in anterior pituitary gland from immature female rats. In the present work, we showed that 17ß-E2 acute treatment exerted opposite effects on the two sGC subunits, increasing 1 and decreasing ß1 subunit protein and mRNA expression. This action on sGC protein expression was maximal 6–9 h after 17ß-E2 administration. 17ß-E2 also caused the same effect on mRNA expression at earlier times. Concomitantly, 17ß-E2 dramatically decreased sGC activity 6 and 9 h after injection. These effects were specific of 17ß-E2, because they were not observed with the administration of other steroids such as progesterone and 17-estradiol. This inhibitory action of 17ß-E2 on sGC also required the activation of estrogen receptor (ER), because treatment with the pure ER antagonist ICI 182,780 completely blocked 17ß-E2 action. 17ß-E2 acute treatment caused the same effects on pituitary cells in culture. These results suggest that 17ß-E2 exerts an acute inhibitory effect on sGC in anterior pituitary gland by down-regulating sGC ß1 subunit and sGC activity in a specific, ER-dependent manner.

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