Abstract
Evidence from clinical and experimental studies suggests that the female population is tolerant to inflammatory and cardiovascular anomalies of endotoxemia. In this study we investigated the possibilities that female rats are also protected against the arterial baroreceptor depressant effect of endotoxemia and that this interaction is modulated by gonadal hormones. The effect of i.v. lipopolysaccharides (LPS, 10 mg/kg) on baroreflex chronotropic activity were assessed in conscious sham‐operated (SO) female rats as well as in ovariectomized (OVX) rats supplemented with or without gonadal hormones. Baroreflex curves relating changes in chronotropic responses to increases or decreases in blood pressure evoked by i.v. doses (1–16 μg/kg) of phenylephrine (PE) and sodium nitroprusside (SNP), respectively, were constructed and slopes of the curves were taken as measures of baroreflex sensitivity (BRSPE, BRSSNP). While LPS had no effect on baroreflex activity tested by PE in SO rats, it caused downward shifts in baroreflex curves generated by SNP and significant reductions (by ~ 25%) in slopes of the curves (BRSSNP). Compared with SO rats, significantly greater reductions in BRSSNP were caused by LPS in OVX rats (~ 50%), inferring a restraining influence for gonadal hormones on LPS‐BRSSNP interaction. The BRSSNP depressant effect of LPS in OVX rats was largely eliminated after supplementation with PPT (estrogen receptor‐α agonist), in contrast to no effect for DPN (estrogen receptor‐β agonist), estrogen, or medroxyprogesterone. Immunohistochemical studies revealed that PPT was more effective than estrogen or DPN in attenuating the LPS‐evoked increases in myocardial expressions of NF‐κB and iNOS in OVX rats. Further, the three estrogenic drugs caused comparable increases in myocardial HSP70 expression in the same rat model. None of these molecular entities was improved by medroxyprogesterone. These findings preferentially implicate antiinflammatory pathways of estrogen receptor‐α in the alleviation of baroreflex dysfunction induced by endotoxemia in female rats.Support or Funding InformationSupported by the Science and Technology Development Fund, Egypt (STDF Grant No. 14895)This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
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