title: Pharmacological characterization of the mechanisms involved in the vasorelaxation induced by progesterone and 17β-estradiol on isolated canine basilar and internal carotid arteries.
abstract: Progesterone and 17β-estradiol induce vasorelaxation through non-genomic mechanisms in several isolated blood vessels; however, no study has systematically evaluated the mechanisms involved in the relaxation induced by 17β-estradiol and progesterone in the canine basilar and internal carotid arteries that play a key role in cerebral circulation. Thus, relaxant effects of progesterone and 17β-estradiol on KCl- and/or PGF2α-pre-contracted arterial rings were investigated in absence or presence of several antagonists/inhibitors/blockers; the effect on the contractile responses to CaCl2 was also determined. In both arteries progesterone (5.6-180 μM) and 17β-estradiol (1.8-180 μM): (1) produced concentration-dependent relaxations of KCl- or PGF2α-pre-contracted arterial rings; (2) the relaxations were unaffected by actinomycin D (10 μM), cycloheximide (10 μM), SQ 22,536 (100 μM) or ODQ (30 μM), potassium channel blockers and ICI 182,780 (only for 17β-estradiol). In the basilar artery the vasorelaxation induced by 17β-estradiol was slightly blocked by tetraethylammonium (10mM) and glibenclamide (KATP; 10 μM). In both arteries, progesterone (10-100 μM), 17β-estradiol (3.1-31 μM) and nifedipine (0.01-1 μM) produced a concentration-dependent blockade of the contraction to CaCl2 (10 μM-10mM). These results suggest that progesterone and 17β-estradiol produced relaxation in the basilar and internal carotid arteries by blockade of L-type voltage dependent Ca(2+) channel but not by genomic mechanisms or production of cAMP/cGMP. Potassium channels did not play a role in the relaxation to progesterone in both arteries or in the effect of 17β-estradiol in the internal carotid artery; meanwhile KATP channels play a minor role on the effect of 17β-estradiol in the basilar artery.
authors: Departamento de Farmacobiología, Cinvestav-Coapa, Czda. de los Tenorios 235, Col. Granjas-Coapa, Deleg. Tlalpan, C.P. 14330, México D.F., Mexico.
authors: Martha B
authors: MB
authors: Ramírez-Rosas
authors: Departamento de Farmacobiología, Cinvestav-Coapa, Czda. de los Tenorios 235, Col. Granjas-Coapa, Deleg. Tlalpan, C.P. 14330, México D.F., Mexico.
authors: Luis E
authors: LE
authors: Cobos-Puc
authors: Departamento de Farmacobiología, Cinvestav-Coapa, Czda. de los Tenorios 235, Col. Granjas-Coapa, Deleg. Tlalpan, C.P. 14330, México D.F., Mexico.
authors: Araceli
authors: A
authors: Sánchez-López
authors: Departamento de Farmacobiología, Cinvestav-Coapa, Czda. de los Tenorios 235, Col. Granjas-Coapa, Deleg. Tlalpan, C.P. 14330, México D.F., Mexico.
authors: Erika J
authors: EJ
authors: Gutiérrez-Lara
authors: Departamento de Farmacobiología, Cinvestav-Coapa, Czda. de los Tenorios 235, Col. Granjas-Coapa, Deleg. Tlalpan, C.P. 14330, México D.F., Mexico. Electronic address: dcenturi@cinvestav.mx.
authors: David
authors: D
authors: Centurión
mesh_terms: D000818:Animals; D001488:Basilar Artery / Q000187:drug effects / Q000502:physiology; D015220:Calcium Channels / Q000378:metabolism*; D002343:Carotid Artery, Internal / Q000187:drug effects / Q000502:physiology; D004958:Estradiol / Q000008:administration & dosage*; D006801:Humans; D009924:Organ Culture Techniques; D015221:Potassium Channels / Q000378:metabolism; D011374:Progesterone / Q000008:administration & dosage*; D015398:Signal Transduction / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects* / Q000502:physiology
chemical_list: D015220:Calcium Channels; D015221:Potassium Channels; D011374:Progesterone; D004958:Estradiol
keywords: 17β-Estradiol; Ca(2+) channels; Cerebral arteries; Progesterone; Vasorelaxation