Acute modulation of Ca2+ influx on rat heart by 17-estradiol

BUITRAGO C; MASSHEIMER V; RUSSO DE BOLAND A

CELLULAR SIGNALLING

ELSEVIER SCIENCE INC

Lugar: Amsterdam; Año: 2000 vol. 12 p. 47 - 52

0898-6568

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 17-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 17α-estradiol, dihydrotestosterone, and progesterone were devoid of activity. The effect of 17-estradiol (5 min, 10-10 M) was suppressed by nitrendipine (1 microM) and LaCl3 (10 M), involving the activation of voltage-dependent Ca2+ channels in the acute increase of rat heart calcium influx by the hormone. 17-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 17-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.