Abstract 617: Bisphenol A Inhibits GPR30-Mediated Dilation of Mesenteric Resistance Arteries

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Abstract

We previously showed that activation of the membrane estrogen receptor GPR30 decreases blood pressure in hypertensive ovariectomized mRen2.Lewis rats and acutely dilates mesenteric resistance arteries. These studies suggest that GPR30 plays a role in estrogen’s beneficial cardiovascular effects. Bisphenol A (BPA) is an endocrine-disrupting chemical found in most manufactured plastic products that also binds to GPR30 in the nanomolar range. Clinical studies show a significant correlation between elevated urinary BPA and increased diagnosis of cardiovascular diseases including hypertension. Therefore, we hypothesized that BPA may disrupt the vasodilatory effects mediated by the novel estrogen receptor GPR30. Second-order mesenteric arteries from 15 week-old Lewis females were denuded and mounted on a wire myograph. Arteries were preconstricted with 10 μM phenylephrine before assessing the response to increasing concentrations of the selective GPR30 agonist G-1 (0.001-3 μM). Pretreatment with 10 μM BPA significantly inhibited G-1-induced relaxation of denuded vessels (Figure, *P<0.01). In summary, BPA blocked the vasodilatory actions of G-1 in vascular smooth muscle, perhaps by competing for GPR30 and/or altering its downstream signaling. We conclude that human exposure to BPA may interfere with the protective estrogenic effects mediated by GPR30.

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