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Advances in experimental medicine and biology

High sugar intake blunts arterial baroreflex via estrogen receptors in perinatal taurine supplemented rats.


PMID 23392952

Abstract

In adult rats, perinatal taurine depletion followed by high sugar intake alters neural and renal control of arterial pressure via the renin-angiotensin system. This study tests the hypothesis that perinatal taurine supplementation predisposes adult female rats to the adverse arterial pressure effect of high sugar intake via the renin-angiotensin system, rather than via estrogen. Female Sprague-Dawley rats were fed normal rat chow with 3% taurine (taurine supplementation, TS) or water alone (control, C) from conception to weaning. Their female offspring were fed normal rat chow with either 5% glucose in tap water (TSG, CG) or tap water alone (TSW, CW). At 7-8 weeks of age, the female offspring's renin-angiotensin system or estrogen receptors were inhibited by captopril or tamoxifen, respectively. Body weight, heart weight, kidney weight, mean arterial pressures (MAP), and heart rates were not significantly different among groups without captopril or tamoxifen. Captopril (but not tamoxifen) decreased MAP but not heart rates in all groups. In TSG compared to TSW, CW, and CG groups, baroreflex sensitivity of heart rate (BSHR) and renal nerve activity (BSRA) were significantly decreased. Neither captopril nor tamoxifen altered BSHR in TSG, but tamoxifen (but not captopril) restored TSG BSRA to CW or CG control levels. Perinatal taurine supplementation did not disturb sympathetic and parasympathetic nerve activity in the adult rats on high or basal sugar intake. Compared to its effect in CW and CG groups, tamoxifen increased sympathetic but decreased parasympathetic activity less in TSG and TSW groups. Inhibition of the renin-angiotensin system did not affect autonomic nerve activity in any group. These data suggest that in adult female rats that are perinatally supplemented with taurine, high sugar intake after weaning blunts arterial baroreflex via an estrogen (but not renin-angiotensin) mechanism.