Abstract
These preliminary data examine the acute affects of medroxyprogesterone acetate (MPA) alone and in combination with estradiol (E2) on conduit vessel responsiveness in young women. We suppressed endogenous estrogens and progesterone in three subjects using a gonadotropin - releasing hormone antagonist (GnRHa) for 14 days. On day 5 of GnRHa, two subjects were administered 0.2 mg E2 for 5 days (GnRH + E2), and on day 10 added 200 mg MPA for 5 days (GnRH + E2 + MPA). One subject was given MPA beginning on day 5 (GnRH + MPA) and added E2 on day 10 (GnRH + MPA + E2). On days 4, 9, and 14 of GnRHa administration, wall tracking of high resolution ultrasound images of the brachial artery were used during flow mediated dilation (FMD) and nitroglycerin (NTG) administration to test endothelial dependent and independent vasodilation, respectively. There was no difference in baseline brachial artery diameter, shear rate, or dilation to NTG between hormone treatments (p>0.05). During treatment with GnRHa + E2, FMD was greater than GnRHa alone (9.87 ± 2.81% vs. 5.65 ± 1.85%; p=.039). FMD decreased with GnRHa + E2 + MPA and was not significantly different from GnRHa alone (4.24 ± 0.02% vs. 5.65 ± 1.85%; p>0.05). In the subject treated with GnRHa + MPA, FMD was similar to GnRHa treatment alone. These preliminary data support previous evidence that E2 increases endothelial dependent vasodilation, and expand upon this finding to suggest that acute MPA administration attenuates the affects of E2 on the vasculature. Supported by the Medical Research Foundation of Oregon
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