Abstract
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 17β-estradiol on Ca 2+ fluxes through second messenger pathways in rat cardiac muscle. Exposure of rat ventricle to low levels of 17β-estradiol (10 −12–10 −8 M) increased 45Ca 2+ 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 17α-estradiol, dihydrotestosterone, and progesterone were devoid of activity. The effect of 17β-estradiol (5 min, 10 −10 M) was suppressed by nitrendipine (1 μM) and LaCl 3 (10 μM), involving the activation of voltage-dependent Ca 2+ channels in the acute increase of rat heart calcium influx by the hormone. 17β-estradiol rapidly increased cAMP content and PKA activity of rat cardiac muscle in parallel to the changes in Ca 2+ uptake. In addition the cAMP antagonist Rp-cAMPS suppressed 17β-estradiol-dependent Ca 2+ influx. Altogether, the data suggest the involvement of the cAMP/PKA messenger system in the nongenomic modulation of Ca 2+ influx in rat cardiac muscle by physiological levels of 17β-estradiol.
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