Acute modulation of Ca2+ influx on rat heart by 17beta-estradiol.
Estrogens initiate their action by binding to specific intracellular receptors and then acting on gene expression. In addition, there is growing evidence of a direct membrane effect via interaction with a cell surphase receptor. The aim of the present study was to investigate the acute effects of 17beta-estradiol on Ca2+ fluxes through second messenger pathways in rat cardiac muscle. Exposure of rat ventricle to low levels of 17beta-estradiol (10(-12)-10(-8) M) increased 45Ca2+ influx within 1 min (+38%); the response was biphasic, peaking at 2 and 5 min (+60 and +55%, respectively). The effect of the hormone on rat heart seems to be specific since 17alpha-estradiol, dihydrotestosterone, and progesterone were devoid of activity. The effect of 17beta-estradiol (5 min, 10(-10) M) was suppressed by nitrendipine (1 microM) and LaCl3 (10 microM), involving the activation of voltage-dependent Ca2+ channels in the acute increase of rat heart calcium influx by the hormone. 17Beta-estradiol rapidly increased cAMP content and PKA activity of rat cardiac muscle in parallel to the changes in Ca2+ uptake. In addition the cAMP antagonist Rp-cAMPS suppressed 17beta-estradiol-dependent Ca2+ influx. Altogether, the data suggest the involvement of the cAMP/PKA messenger system in the nongenomic modulation of Ca2+ influx in rat cardiac muscle by physiological levels of 17beta-estradiol.
Buitrago
C
C
Departamento de Biologia, Bioquimica & Farmacia, Universidad Nacional del Sur, San Juan, Bahia Blanca, Argentina.
Massheimer
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V
de Boland
A R
AR
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D004958:Estradiol / Q000494:pharmacology*; D005260:Female; D066298:In Vitro Techniques; D017136:Ion Transport / Q000187:drug effects; D009206:Myocardium / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D015398:Signal Transduction / Q000187:drug effects*
D004958:Estradiol; D002118:Calcium