Objective To explore the mechanism of vascular function by maternal exposure to lipopolysaccharide in adult offspring rats.
Methods Nulliparous pregnant and time-matched SD rats were randomly divided into two groups control group and LPS group (n = 6 for each group). Saline or LPS (0.79 mg/kg) were administered intraperitoneally on the pregnant day 8, 10 and 12. All offspring rats were weaned at 4 weeks of age. Bloodpressure was measured noninvasively by the tail-cuff method at 9, 11, 13 and 15 weeks of age. Mesenteric vascular reactivity in response to angiotensin II (Ang II, 10–10–10–5 mol/L) and protein level of angiotensin II1 receptor (AT1R) were determined by Westen blot, respectively.
Results The systolic blood pressure in the postnatal offsprings treated with LPS rats was higher than control group at 9, 11, 13 and 15 weeks of age (109.6 ± 2.6 vs 102.9 ± 2.5,117.7 ± 1.5 vs 108.1 ± 3.3,128.1 ± 3.6 vs 117.2 ± 2.1,135.1 ± 3.2 vs 123.0 ± 2.3)mm Hg, respectively, all p < 0.01), the maximum constriction response to Ang II in the third-order branches of mesenteric arteries ((8.5 ± 0.4) vs (3.5 ± 0.3)mN,) and the AT1 receptor expression of mesenteric arteries (1.21 ± 0.08 vs 0.75 ± 0.08) were increased at the age of 15 weeks in rat offsprings after maternal exposure to LPS.
Conclusion The increased AT1 receptor expression and augmented response to Ang II are involved in the pathogenesis of hypertension in the adult rat offsprings following maternal exposure to LPS.
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