Taurine supplementation reduces renal nerve activity in male rats in which renal nerve activity was increased by a high sugar diet

Academic Article

Abstract

  • © 2017, Springer Science+Business Media B.V. This study tests the hypothesis that taurine supplementation reduces sugar-induced increases in renal sympathetic nerve activity related to renin release in adult male rats. After weaning, male rats were fed normal rat chow and drank water containing 5% glucose (CG) or water alone (CW) throughout the experiment. At 6–7 weeks of age, each group was supplemented with or without 3% taurine in drinking water until the end of experiment. At 7–8 weeks of age, blood chemistry and renal nerve activity were measured in anesthetized rats. Body weights slightly and significantly increased in CG compared to CW groups but were not significantly affected by taurine supplementation. Plasma electrolytes except bicarbonate, plasma creatinine, and blood urea nitrogen were not significantly different among the four groups. Mean arterial pressure significantly increased in both taurine treated groups compared to CW, while heart rates were not significantly different among the four groups. Further, all groups displayed similar renal nerve firing frequencies at rest and renal nerve responses to sodium nitroprusside and phenylephrine infusion. However, compared to CW group, CG significantly increased the power density of renin release-related frequency component, decreased that of sodium excretion-related frequency component, and decreased that of renal blood flow-related frequency component. Taurine supplementation completely abolished the effect of high sugar intake on renal sympathetic activity patterns. These data indicate that in adult male rats, high sugar intake alters the pattern but not firing frequency of sympathetic nerve activity to control renal function, and this effect can be improved by taurine supplementation.
  • Authors

    Digital Object Identifier (doi)

    Pubmed Id

  • 19620544
  • Author List

  • Rakmanee S; Kulthinee S; Wyss JM; Roysommuti S
  • Start Page

  • 27
  • End Page

  • 37
  • Volume

  • 975