Short‐term estrogen depletion does not promote hypertension in mice

Abstract

Our lab has previously demonstrated that estrogen (E2) downregulates the expression and function of voltage‐gated, L‐type Ca2+ channels (CaL) in coronary arteries in vitro. In this study we hypothesized that the in vivo depletion of E2 would generate an increase in Ca2+‐dependent arterial tone. Mice (C57BL/6) underwent an ovariectomy (OVX) or sham surgery at 8‐wks of age. Biotelemetry measured a drop in heart rate (p=0.002) and blood pressure (p=0.09) in OVX mice within 2‐wks post‐surgery suggesting a baroreceptor reflex compensation. Mice were sacrificed 4‐wks post‐surgery and the mesenteric arteries isolated. The OVX mice demonstrated atrophied uteri and low E2 plasma levels. In the mesenteric arteries, Western blots demonstrated a slight (p=0.12) increase in CaL expression from OVX mice. Mesenteric arterial reactivity experiments indicated no difference between groups in their spontaneous tone and response to the CaL agonist, FPL64176 (3×10−7 to 1×10−6). This suggests that, while E2 depletion alone does not promote hypertension, other underlying pathologies in conjunction with E2 depletion may lead to hypertension and other cardiovascular diseases. Support: NIGMM of the NIH, Grant #P20 GM103429–11