The present study investigates the effect of perinatal taurine exposure on renal function in adult, female rats on a high sugar diet. Perinatal taurine depleted (TD), supplemented (TS) or untreated control (C) female offspring were fed normal rat chow and tap water (CW,TDW or TSW) or tap water with 5% glucose (CG, TDG or TSG) after weaning. At 7-8 weeks of age, renal function was studied in the conscious, restrained rats. Mean arterial pressure was significantly higher in TDW, TDG, and TSG rats. Plasma sodium concentration was significantly lower in all glucose treated animals, but the greatest decrease was in TDW rats. Basal renal blood flow was lowest in TSW and TSG, and the responses to a saline load were also lowest in those two groups. These changes were consistent with increased renal vascular resistance. The basal glomerular filtration rate was lowest in TSW, but the responses to a saline load were similar in all of the groups. Water excretion was lower in TSG and TSW, consistent with increased renal tubular water reabsorption. These data suggest that perinatal taurine exposure alters normal renal function and renal responses to dietary sugar in adult female offspring.
This study tests the hypothesis that perinatal taurine depletion produces autonomic nervous system dysregulation and increases arterial pressure in young male rats on a high sugar diet. Sprague-Dawley dams were taurine depleted (beta-alanine 3% in water) or untreated from conception to weaning. Their male offspring were fed normal rat chow with or without 5% glucose. At 7-8 weeks of age, male offspring were tested in a conscious, unrestrained or an anesthetic state. Body weight was slightly lower in the taurine-depleted rats with similar heart or kidney to body weight ratios. Plasma potassium, blood urea nitrogen, plasma creatinine, hematocrit, fasting blood glucose concentrations and glucose tolerance were all similar. In the taurine-depleted, high glucose group, mean arterial pressure and sympathetic nervous system activity were increased and baroreflex function was impaired. These findings suggest that perinatal taurine depletion causes autonomic nervous system dysfunction that may contribute to dietary high sugar-induced hypertension in this model.
Taurine is an abundant free amino acid found in mammalian cells that contributes to many physiologic functions from that of a simple cell osmolyte to a programmer of adult health and disease. Taurine’s contribution extends from conception throughout life, but its most critical exposure period is during perinatal life. In adults, taurine supplementation prevents or alleviates cardiovascular disease and related complications. In contrast, low taurine consumption coincides with increased risk of cardiovascular disease, obesity and type II diabetes. This review focuses on the effects that altered perinatal taurine exposure has on long-term mechanisms that control adult arterial blood pressure and could thereby contribute to arterial hypertension through its ability to program these cardiovascular regulatory mechanisms very early in life. The modifications of these mechanisms can last a lifetime and transfer to the next generation, suggesting that epigenetic mechanisms underlie the changes. The ability of perinatal taurine exposure to influence arterial pressure control mechanisms and hypertension in adult life appears to involve the regulation of growth and development, the central and autonomic nervous system, the renin-angiotensin system, glucose-insulin interaction and changes to heart, blood vessels and kidney function.
This study tests the hypothesis that perinatal taurine supplementation prevents diabetes mellitus and hypertension in adult offspring of maternal diabetic rats. Female Wistar rats were fed normal rat chow and tap water with (Diabetes group) or without diabetic induction by intraperitoneal streptozotocin injection (Control group) before pregnancy. Then, they were supplemented with 3% taurine in water (Control+T and Diabetes+T groups) or water alone from conception to weaning. After weaning, both male and female offspring were fed normal rat chow and tap water throughout the study. Blood chemistry and cardiovascular parameters were studied in 16-week old rats. Body, heart, and kidney weights were not significantly different among the eight groups. Further, lipid profiles except triglyceride were not significantly different among male and female groups, while male Diabetes displayed increased fasting blood glucose, decreased plasma insulin, and increased plasma triglyceride compared to other groups. Compared to Control, mean arterial pressures significantly increased and baroreflex control of heart rate decreased in both male and female Diabetes, while heart rates significantly decreased in male but increased in female Diabetes group. Although perinatal taurine supplementation did not affect any measured parameters in Control groups, it abolished the adverse effects of maternal diabetes on fasting blood glucose, plasma insulin, lipid profiles, mean arterial pressure, heart rate, and baroreflex sensitivity in adult male and female offspring. The present study indicates that maternal diabetes mellitus induces metabolic and cardiovascular defects more in male than female adult offspring, and these adverse effects can be prevented by perinatal taurine supplementation.
Lifetime treatment with oral captopril prevents the development of hypertension in spontaneously hypertensive rats (SHR). We tested the hypothesis that this treatment also prevents the hypertensive response that occurs when untreated NaCl-sensitive SHR are placed on a high NaCl diet. Female SHR were continuously treated with oral captopril before conception and throughout lactation, and the offspring were similarly treated with oral captopril throughout life. At 6 weeks of age, treated male SHR were placed on an 8% (or remained on a 1%) NaCl diet, and systolic arterial pressure, heart rate, and body weight were monitored for 2 weeks. The 8% NaCl diet caused a rapid increase in arterial pressure in the lifetime captopril-treated rats, and 18 days after the initiation of the diet, the mean arterial pressure of this group was 136±7 mm Hg compared with 100±2 mm Hg in the 1% NaCl diet rats. The results of a second experiment confirmed the hypertensive effect of the high NaCl diet in lifetime captopril-treated SHR and demonstrated that after 18 days on M any clinical and experimental studies suggest that the renin-angiotensin system plays an important role in the pathogenesis of hypertension. Some of the strongest experimental evidence supporting this hypothesis is derived from studies that have administered angiotensin-converting enzyme (ACE) inhibitors (eg, captopril) peripherally or into the cerebral ventricles of spontaneously hypertensive rats (SHR), 13 although some authors have not found a decrease in arterial pressure in SHR given intracerebroventricular captopril. 4 ' 5 Systemic (and in several experiments intracerebroventricular) administration of the inhibitors results in a reduction in arterial pressure and a significant alteration in brain angiotensin II (Ang II) and ACE activity. Recent studies have demonstrated that early exposure of SHR to ACE inhibitors causes a permanent reduction in arterial pressure even after the ACE inhibition is stopped later in life 6 ' 7 and that administration of ACE inhibitors to SHR from conception onward (lifetime treatment) prevents the development of hypertension in SHR. 8 This antihypertensive effect appears to be due in part to alteration in the endogenous renin-angiotensin system in the brain, re-
Perinatal taurine depletion leads to several physiological impairments in adult life, in part, due to taurine’s effects on the renin-angiotensin system, a crucial regulator of growth and differentiation during early life. The present study tests the hypothesis that perinatal taurine depletion predisposes adult female rats to impaired baroreceptor control of arterial pressure by altering the renin-angiotensin system. Female Sprague Dawley (SD) rats were fed normal rat chow and from conception to weaning drank 3% beta-alanine in water (taurine depletion, TD) or water alone (Control, C). Female offspring ate a normal rat chow and drank water with (G) or without (W) 5% glucose throughout the experiment. To test the possible role of the renin-angiotensin system, 50% of the rats received captopril (an angiotensin converting enzyme inhibitor, 400 mg/L) from 7 days before parameter measurements until the end of experiment. At 7-8 weeks of age, arterial pressure, heart rate, baroreflex control of heart rate and renal nerve activity were studied in either conscious, freely moving or anesthetized rats. Perinatal taurine depletion did not alter resting mean arterial pressure or heart rate in the adult female offspring that received either high or normal sugar intake. Captopril treatment slightly decreased mean arterial pressure but not heart rate in all groups. Compared to controls, only the TDG rats displayed blunted baroreflex responses. Captopril treatment normalized baroreflex sensitivity in TDG. The present data indicate that in perinatal taurine depleted female rats, the renin-angiotensin system underlines the ability of high sugar intake to blunt baroreceptor responses.
The present study tests the sex-dependent effect of perinatal taurine exposure on arterial pressure control in adults. Female Sprague-Dawley rats were fed normal rat chow with 3% beta-alanine (taurine depletion, TD), 3% taurine (taurine supplementation, TS) or water alone (C) from conception to weaning. Their male and female offspring were then fed normal rat chow and tap water with 5% glucose (C with glucose, CG; TD with glucose, TDG; TS with glucose, TSG) or water alone (CW, TDW or TSW). At 7-8 weeks of age, they were studied in a conscious condition. Body weights were lower in male and female TDG and male TDW rats. Kidney to body weights increased in female TSW but not TSG. Plasma sodium and potassium were not significantly different among males. In the females, plasma sodium levels were lower in all glucose treated groups while plasma potassium levels were lower only in TDG. Hematocrit, fasting blood glucose, and glucose tolerance were not significantly different among sexes. Mean arterial pressures increased in male TDG, TSW, and TSG while in the females, mean arterial pressures increased in TDW, TDG, and TSG. Heart rates were not significantly different among sexes. The present data indicate that perinatal exposure alters arterial pressure control of adult rats and this effect is gender specific.
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