Abstract
Perinatal taurine exposure has long-term effects on the arterial pressure and renal function. This study tests its influence on renal potassium excretion in young adult, conscious rats. Female Sprague-Dawley rats were fed normal rat chow and given water alone (C), 3% beta-alanine in water (taurine depletion, TD) or 3% taurine in water (taurine supplementation, TS), either from conception until delivery (fetal period; TDF or TSF) or from delivery until weaning (lactation period; TDL or TSL). In Experiment 1, male offspring were fed normal rat chow and tap water, while in Experiment 2, beta-alanine and taurine were treated from conception until weaning and then female pups were fed normal rat chow and 5% glucose in drinking water (CG, TDG or TSG) or water alone (CW, TDW or TSW). At 7-8 weeks of age, renal potassium excretion was measured at rest and after an acute saline load (5% of body weight) in conscious, restrained rats. Although all male groups displayed similar renal potassium excretion, TSF rats slightly increased fractional potassium excretion at rest but not in response to saline load, whereas TDF did the opposite. Plasma potassium concentration was only slightly altered by the diet manipulations. In female offspring, none of the perinatal treatments significantly altered renal potassium excretion at rest or after saline load. High sugar intake slightly decreased potassium excretion at rest in TDG and TSG, but only the TDG group displayed a decreased response to saline load. The present data indicates that perinatal taurine exposure only mildly influences renal potassium excretion in adult male and female rats.
Highlights
Perinatal taurine depletion induces low birth weight, multiple organ damage and low tissue taurine content in many organs and in plasma [1,2], but the mechanisms underlying these adverse effects remain ambiguous
After an acute saline load, plasma potassium slightly decreased in controls and remained at these levels throughout the study
Potassium excretion at rest and after a saline load decreased only in TDG when compared to CW, CG, and TSG (Fig. 5)
Summary
Perinatal taurine depletion induces low birth weight, multiple organ damage and low tissue taurine content in many organs and in plasma [1,2], but the mechanisms underlying these adverse effects remain ambiguous. Diabetes mellitus, hypertension, and obesity are inversely correlated with body taurine content [3]. Taurine supplementation appears to prevent some aspects of age-related renal damage, sugar-induced hypertension, ethanol-induced hypertension and drug-induced diabetes. Perinatal taurine supplementation can prevent cardiovascular diseases in the adult offspring following maternal malnutrition [4,5] and in spontaneously hypertensive rats [6,7]. Our previous experiments indicate that perinatal taurine or potassium depletion decreases taurine concentration in this area [19], disturbing renal urine concentration and dilution mechanisms. Taurine increases renal sodium excretion [21], but it influences on renal potassium excretion is not well known
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