We investigated the effects of 17 beta-estradiol (beta E(2)), alpha-es
tradiol (alpha E(2)), and progesterone (P) on baseline and vasopressin
(AVP)-induced [Ca2+](i) in human platelets obtained from healthy male
and female volunteers. Platelets were treated with beta E(2), alpha E
(2), P, or ethanol vehicle for 30 min at 37 degrees C. In males, both
beta E(2) and P at 10(-5) mol/L reduced the AVP-induced rise in [Ca2+]
(i), to 72 +/- 3% (mean +/- SEM) and 53 +/- 3%, respectively. However,
at 10(-6) mol/L only PE, had a significant effect (P < .02). In femal
es, 10(-6) and 10(-5) beta E(2) reduced the AVP response to 85.3 +/- 4
.6% and 80.8 +/- 5.4% of control values, respectively. Progesterone (1
0(-6) and 10(-5) mol/L) reduced the AVP response to 83.8 +/- 5.1% and
60.3 +/- 2.0% of control values, respectively. The inactive estrogen (
alpha E(2) had no effect on basal or AVP-induced rise in [Ca2+](i) in
either subject population, suggesting hormonal specificity. Neither be
ta E(2) nor P affected baseline [Ca2+](i) in either population. Thus,
by attenuating [Ca2+](i) responses in platelets, beta E(2) and P may m
odulate platelet aggregation and atherosclerosis.