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1 Magee-Womens Research Institute and Department of Obstetrics, Gynecology and Reproductive Sciences, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213; 2 School of Pharmacy, Division of Pharmaceutical Sciences, University of Missouri, Kansas City, Missouri 64110; and 3 College of St. Catherine, Saint Paul, Minnesota 55105
Supraphysiological
increases in serum triglycerides and cholesterol often occur during
pregnancy, but their effects on vascular function are poorly
understood. Intraperitoneal injection of the nontoxic surfactant
poloxamer 407 (P-407) results in sustained elevation of triglycerides
and cholesterol. We asked if P-407-induced hyperlipidemia during late
pregnancy adversely affects mesenteric resistance artery vasodilator
function. On days 13-15 of pregnancy, rats were given a
single intraperitoneal injection of P-407, sterile water vehicle, or
non-lipid-altering pluronic F-88 (P-88). Four days postinjection, serum
triglycerides, cholesterol, free fatty acids, and the lipid
peroxidation product malondialdehyde were significantly increased in
P-407-treated rats. Mesenteric arteries from P-407-treated rats
displayed significant increases in myogenic reactivity (constrictor
responses to step increases in intraluminal pressure). The nitric oxide
(NO) blocker N
-methyl-L-arginine
increased the myogenic response in control but not in P-407 arteries,
normalizing group differences. Endothelial removal increased myogenic
reactivity beyond that of prior NO synthase inhibition in controls and
potentiated myogenic reactivity in P-407 arteries such that responses
again converged. Relaxation responses to the endothelium-dependent
vasodilator methacholine did not differ. We conclude that that
P-407-induced hyperlipidemia during pregnancy increases myogenic
reactivity due to selective attenuation of an NO-mediated vasodilator
component of the myogenic response.
pregnancy; poloxamer 407; triglyceride; malondialdehyde; resistance vasculature
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