TY  - JOUR
AU  - Díaz, M.
AU  - Ramírez, C.M.
AU  - Marin, R.
AU  - Marrero-Alonso, J.
AU  - Gómez, T.
AU  - Alonso, R.
T1  - Acute relaxation of mouse duodenun by estrogens: Evidence for an estrogen receptor-independent modulation of muscle excitability
LA  - eng
PY  - 2004
SP  - 161
EP  - 178
T2  - European Journal of Pharmacology
SN  - 0014-2999
VL  - 501
IS  - 1-3
AB  - 17-β-Estradiol, the stereoisomer 17-α-estradiol and the synthetic estrogen diethylstilbestrol (DES), all caused a rapid (<3 min) dose-dependent reversible relaxation of mouse duodenal spontaneous activity, reduced basal tone and depressed the responses to CaCl 2 and KCl. The steroidal antiestrogen 7α-[9-[(4,4,5,5,5,-pentafluoropenty)sulphinyl] nonyl]-estra-1,3,5(19)-triene-3,17β-diol (ICI182,780) failed to either mimic or prevent the effect of 17-β-estradiol. The effect of estrogens was unrelated to activation of nitric oxide (NO), mitogen-activated protein kinase (MAPK), protein kinase A (PKA), protein kinase G (PKG) or protein kinase C (PKC). Estrogen-induced relaxation was partially reversed by 1,4-dihydro-2,6-dimethyl-5-nitro-4-[2-(trifluoromethyl)phenyl] -pyridine-3-carboxilic acid methyl ester (BAY-K8644), depolarization, or by application of tetraethylammonium or 4-aminopyridine, but not by glibenclamide, apamin, charybdotoxin, paxilline or verruculogen. The effects of BAY-K8644 and K + channel blockers were synergistic, and allowed relaxed tissues to recover spontaneous activity and basal tone. We hypothesize that the rapid non-genomic spasmolytic effect of estrogens on mouse duodenal muscle might be triggered by an estrogen-receptor-independent mechanism likely involving activation of tetraethylamonium- and 4-aminopyridine-sensitive K + channels and inhibition of L-type Ca2 + channels on the smooth muscle cells. © 2004 Elsevier B.V. All rights reserved.
DO  - 10.1016/j.ejphar.2004.08.020
UR  - https://portalciencia.ull.es/documentos/5e39b7ba2999523aa92715d0
DP  - Dialnet - Portal de la Investigación
ER  -