Abstract
Reductions in uterine perfusion pressure are central to the pathogenesis of preeclampsia and may trigger increased production of vasoconstrictor prostanoids such as thromboxane (TX). This may lead to the altered maternal vascular reactivity observed in preeclampsia. The purpose of this study is to determine the impact of TX on resistance artery vascular behavior after reductions in uterine perfusion pressure in gravid rats. Pregnant dams were subjected to periodic (Occluder) and chronic (RUPP) reductions in uterine perfusion pressure on GD 14 and compared to SHAM operated controls. On GD 21, resistance‐sized mesenteric arteries were investigated using a pressurized arteriograph where myogenic reactivity and TX constriction were analyzed. Myogenic reactivity was increased to a similar degree in mesenteric arteries from Occluder and RUPP rats compared to SHAM (p<0.05). Pretreatment of arteries with meclofenamate (non‐specific COX inhibitor) or SQ29548 (TX receptor antagonist) ameliorated the increased myogenic reactivity in Occluder and RUPP arteries (p<0.05). Vasoconstriction with U‐46619 was increased in mesenteric arteries from Occluder and RUPP compared to SHAM (p<0.05). These data provide evidence that the vasoconstrictor prostanoids such as TXA2 at least partially mediates the maternal vascular dysfunction that occurs in response to reduced uterine perfusion during pregnancy.
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