Examination of Taurine Chloramine and Taurine on LPS-Induced Acute Pulmonary Inflammatory in Mice.

The novel coronavirus disease (COVID-19), which is prevalent in the world, develops severe pneumonia, of which 30% have fatal acute respiratory distress and acute lung injury. At present, there is no established treatment method for ARDS, and it is desired to develop a therapeutic drug as soon as possible. While TauCl has been reported to have anti-inflammatory effects on culture cells, little information is available concerning in vivo experiments. In the present study, we evaluated the anti-inflammatory effect of taurine chloramine (TauCl), a taurine derivative, against LPS-induced pneumonia in mouse. The mice were pretreated with TauCl intraperitoneally before intratracheal administration of LPS. Additionally, we evaluated the effect of taurine treatment by maintaining the mice on drinking water containing 0.5% taurine. Two days after LPS injection, body weight was decreased by 9.5 %, while lung weight was increased due to the infiltration of inflammatory cells; TauCl attenuated the gain in lung weight. LPS-induced acute pneumonia caused an increase in cytokine/chemokine mRNA expression, including that of IL-1ß, -6, -17, TNF-α, and MCP-1. However, TauCl treatment attenuated IL-6 expression, but not that of the others although the induction of plasma IL-6 tended to be reduced by TauCl treatment. Importantly, a similar effect against LPS-induced acute lung inflammation was confirmed by taurine pretreatment. These findings suggest that TauCl treatment partially prevents IL-6 production induced by acute pneumonia in vivo.

Differences Between Physiological and Pharmacological Actions of Taurine.

In many experimental studies, pharmacological levels of taurine have been used to study physiological functions of taurine. However, this approach is unlikely to be fruitful, as pharmacological administration increases extracellular taurine, while physiological actions of taurine require alterations in intracellular taurine. Recognizing that different mechanisms might underlie the pharmacological and physiological actions of taurine, cardiac properties before and after exposure to various extracellular or intracellular concentrations of taurine were examined. To assess the effect of physiological taurine, myocardial contractility and metabolic status were compared in hearts containing different intracellular taurine concentrations. By contrast, the pharmacological actions of taurine were assessed in normal hearts perfused with buffer containing or lacking 10 mM taurine. Both pharmacological and physiological taurine increased contractile function and oxygen consumption. Yet, the pharmacological actions of taurine on contractile function were dependent on the L-type Ca2+ channel, while the sarcoplasmic reticular Ca2+ ATPase contributed to the physiological actions of taurine. ATP generation from available substrates, glucose, fatty acids, and acetate was increased for both the physiological and pharmacological actions of taurine. However, taurine supplementation enhanced ATP generation by elevating respiratory chain complex I activity and by stimulating metabolic flux through reductions in the NADH/NAD+ ratio, while the pharmacological actions of taurine can be traced to elevations in [Ca2+]i and the observed positive inotropic effect. Thus, the mechanisms underlying the pharmacological actions of taurine on contractile function and energy metabolism are entirely different than those contributing to the physiological actions of taurine.

Bioavailability of Tauropine After Oral Ingestion in Mouse.

In the present study, we investigated the pharmacokinetics of oral ingested tauropine which is a natural taurine derivative found in marine invertebrates, such as abalone, and in mouse. To measure tauropine in the blood, it was derivatized with phenyl isothiocyanate (PITC), and PITC-tauropine was separated by reverse-phase high-performance liquid chromatography (HPLC) and detected by ultraviolet absorbance. Tauropine was detectable in the blood obtained from mice intraperitoneally injected with tauropine. However, it was not detectable in blood obtained from orally treated mice. In conclusion, oral ingested tauropine may be poorly absorbed by the gastrointestinal tract and transported into the blood.

Taurine suppresses liquid-liquid phase separation of lysozyme protein.

Taurine is a compatible osmolyte that confers stability to proteins. Recent studies have revealed that liquid-liquid phase separation (LLPS) of proteins underlie the formation of membraneless organelles in cells. In the present study, we evaluated the role of taurine on LLPS of hen egg lysozyme. We demonstrated that taurine decreases the turbidity of the polyethylene glycol-induced crowding solution of lysozyme. We also demonstrated that taurine attenuates LLPS-dependent cloudiness of lysozyme solution with 0.5 or 1 M NaCl at a critical temperature. Moreover, we observed that taurine inhibits LLPS formation of a heteroprotein mix solution of lysozyme and ovalbumin. These data indicate that taurine can modulate the formation of LLPS of proteins.

The Role of Taurine in Mitochondria Health: More Than Just an Antioxidant.

Taurine is a naturally occurring sulfur-containing amino acid that is found abundantly in excitatory tissues, such as the heart, brain, retina and skeletal muscles. Taurine was first isolated in the 1800s, but not much was known about this molecule until the 1990s. In 1985, taurine was first approved as the treatment among heart failure patients in Japan. Accumulating studies have shown that taurine supplementation also protects against pathologies associated with mitochondrial defects, such as aging, mitochondrial diseases, metabolic syndrome, cancer, cardiovascular diseases and neurological disorders. In this review, we will provide a general overview on the mitochondria biology and the consequence of mitochondrial defects in pathologies. Then, we will discuss the antioxidant action of taurine, particularly in relation to the maintenance of mitochondria function. We will also describe several reported studies on the current use of taurine supplementation in several mitochondria-associated pathologies in humans.

Taurine-Conjugated Metabolites in Hearts.

Mammalian tissues, especially the heart, contain high concentrations of taurine, a beta-amino acid that possesses a variety of physiological functions. While it is well known that taurine reacts with several metabolites, such as bile acids and fatty acids, taurine-conjugated metabolites in the heart have not been specifically studied. Recently, we performed Liquid chromatography-mass spectrometry- (LC-MS-) based metabolome analysis, comparing metabolome profiles of hearts from taurine transporter knockout (TauTKO) mice and wild-type mice to identify differences in taurine-conjugated metabolite content of the two phenotypes. Comparison of the metabolite profiles revealed taurine-containing dipeptides, such as glutamyltaurine, which are present in wild-type but not in TauTKO hearts. These data suggest that taurine functions not only as a free osmolyte but also as a conjugated metabolite within the heart.

Tissue Taurine Depletion Induces Profibrotic Pattern of Gene Expression and Causes Aging-Related Cardiac Fibrosis in Heart in Mice.

Dietary taurine deficiency results in dilated cardiomyopathy in cats while in mice taurine deficiency produced by knocking out the taurine transporter (TauT) gene leads to a reduction in cardiac function with advancing age. The present study elucidated the involvement of cardiac fibrosis in the aging-dependent cardiac disorder of the TauT-knockout (TauTKO) mouse. Old (18-24-month-old) TauTKO mice, but not young (3-5-month-old) mice, exhibit cardiac fibrosis. Transcriptome microarray analysis revealed an increase in pro-fibrotic genes, such as S100A4, ACTA2 and CTGF, in both young and old TauTKO hearts. Based on transcriptome-pathway analysis the genes involved in "organization of extracellular matrix," such as LGALS3, are enriched in old TauTKO hearts compared to old wild-type hearts, suggesting the contribution of these genes to fibrosis. In conclusion, taurine depletion predisposes the heart to fibrosis, which leads to cardiac fibrosis upon aging.

Induction of Growth Differentiation Factor 15 in Skeletal Muscle of Old Taurine Transporter Knockout Mouse.

It has been identified that skeletal muscle is an endocrine tissue. Since skeletal muscle aging affects not only to muscle strength and function but to systemic aging and lifespan, myokines secreted from skeletal muscle may be crucial factors for intertissue communication during aging. In the present study, we investigated the expression of myokines associated with skeletal muscle aging in taurine transporter knockout (TauTKO) mice, which exhibit the accelerated skeletal muscle aging. Among transforming growth factor (TGF)-beta family genes, only growth and differentiation factor 15 (GDF15) was markedly higher (>3-fold) in skeletal muscle of old TauTKO mice compared with that of either young TauTKO mice or old wild-type mice. Circulating levels of GDF15 were also elevated in old TauTKO mice. An elevation in circulating GDF15 was also observed in very old (30-month-old) wild-type mice, while skeletal GDF15 levels were normal. The treatment of cultured mouse C2C12 myotubular cells with aging-related factors that mediate cellular stresses, such as oxidative stress (hydrogen peroxide) and endoplasmic reticulum stress (tunicamycin and thapsigargin), leads to an increase in GDF15 secretion. In conclusion, GDF15 is a myokine secreted by aging-related stress and may control aging phenotype.

Beta-Catenin and SMAD3 Are Associated with Skeletal Muscle Aging in the Taurine Transpoeter Knockout Mouse.

Tissue taurine depletion mediated by knocking out the taurine transporter causes several skeletal muscle abnormalities, including acceleration of cellular aging. In the present study, we investigated the signaling pathway involved in the acceleration of skeletal muscle aging by tissue taurine depletion using the bioinformatic approach of transcriptome data. We previously performed transcriptome analysis on skeletal muscle of taurine transporter knockout (TauTKO) mice using DNA microarray. Bioinformatic analysis of transcriptome data predicted the activation of SMAD3 and ß-catenin as upstream signaling molecules of cyclin-dependent kinase inhibitor 2A (CDKN2A, also called p16INK4A), which is a biomarker gene of cellular senescence. The activation of SMAD3 and ß-catenin in old TauTKO muscle was verified by western blot analysis. These data indicate that SMAD3- and ß-catenin-dependent induction occurs in the TauTKO mouse.

Impaired energy metabolism of the taurine­deficient heart.

Taurine is a ß-amino acid found in high concentrations in excitable tissues, including the heart. A significant reduction in myocardial taurine content leads to the development of a unique dilated, atrophic cardiomyopathy. One of the major functions of taurine in the heart is the regulation of the respiratory chain. Hence, we tested the hypothesis that taurine deficiency-mediated defects in respiratory chain function lead to impaired energy metabolism and reduced ATP generation. We found that while the rate of glycolysis was significantly enhanced in the taurine-deficient heart, glucose oxidation was diminished. The major site of reduced glucose oxidation was pyruvate dehydrogenase, an enzyme whose activity is reduced by the increase in the NADH/NAD+ ratio and by decreased availability of pyruvate for oxidation to acetyl CoA and changes in [Mg2+]i. Also diminished in the taurine-deficient heart was the oxidation of two other precursors of acetyl CoA, endogenous fatty acids and exogenous acetate. In the taurine-deficient heart, impaired citric acid cycle activity decreased both acetate oxidation and endogenous fatty acid oxidation, but reductions in the activity of the mitochondrial transporter, carnitine palmitoyl transferase, appeared to also contribute to the reduction in fatty acid oxidation. These changes diminished the rate of ATP production, causing a decline in the phosphocreatine/ATP ratio, a sign of reduced energy status. The findings support the hypothesis that the taurine-deficient heart is energy starved primarily because of impaired respiratory chain function, an increase in the NADH/NAD+ ratio and diminished long chain fatty acid uptake by the mitochondria. The results suggest that improved energy metabolism contributes to the beneficial effect of taurine therapy in patients suffering from heart failure.

Mitochondrial defects associated with ß-alanine toxicity: relevance to hyper-beta-alaninemia.

Hyper-beta-alaninemia is a rare metabolic condition that results in elevated plasma and urinary ß-alanine levels and is characterized by neurotoxicity, hypotonia, and respiratory distress. It has been proposed that at least some of the symptoms are caused by oxidative stress; however, only limited information is available on the mechanism of reactive oxygen species generation. The present study examines the hypothesis that ß-alanine reduces cellular levels of taurine, which are required for normal respiratory chain function; cellular taurine depletion is known to reduce respiratory function and elevate mitochondrial superoxide generation. To test the taurine hypothesis, isolated neonatal rat cardiomyocytes and mouse embryonic fibroblasts were incubated with medium lacking or containing ß-alanine. ß-alanine treatment led to mitochondrial superoxide accumulation in conjunction with a decrease in oxygen consumption. The defect in ß-alanine-mediated respiratory function was detected in permeabilized cells exposed to glutamate/malate but not in cells utilizing succinate, suggesting that ß-alanine leads to impaired complex I activity. Taurine treatment limited mitochondrial superoxide generation, supporting a role for taurine in maintaining complex I activity. Also affected by taurine is mitochondrial morphology, as ß-alanine-treated fibroblasts undergo fragmentation, a sign of unhealthy mitochondria that is reversed by taurine treatment. If left unaltered, ß-alanine-treated fibroblasts also undergo mitochondrial apoptosis, as evidenced by activation of caspases 3 and 9 and the initiation of the mitochondrial permeability transition. Together, these data show that ß-alanine mediates changes that reduce ATP generation and enhance oxidative stress, factors that contribute to heart failure.

Role of protein phosphorylation in excitation-contraction coupling in taurine deficient hearts.

Taurine is a beta-amino acid found in very high concentration in the heart. Depletion of these intracellular stores results in the development of cardiomyopathy, thought to be mediated by abnormal sarcoplasmic reticular (SR) Ca(2+) transport. There is also evidence that taurine directly alters the Ca(2+) sensitivity of myofibrillar proteins. Major regulators of SR Ca(2+) ATPase (SERCA2a) are the phosphorylation status of a regulatory protein, phospholamban, and SERCA2a expression, which are diminished in the failing heart. The failing heart also exhibits reductions in myofibrillar Ca(2+) sensitivity, a property regulated by the phosphorylation of the muscle protein, troponin I. Therefore, we tested the hypothesis that taurine deficiency leads to alterations in SR Ca(2+) ATPase activity related to reduced phospholamban phosphorylation and expression of SERCA2a. We found that a sequence of events, which included elevated protein phosphatase 1 activity, reduced autophosphorylation of CaMKII, and reduced phospholamban phosphorylation, supports the reduction in SR Ca(2+) ATPase activity. However, the reduction in SR Ca(2+) ATPase activity was not caused by reduced SERCA2a expression. Taurine transporter knockout (TauTKO) hearts also exhibited a rightward shift in the Ca(2+) dependence of the myofibrillar Ca(2+) ATPase, a property that is associated with an elevation in phosphorylated troponin I. The findings support the observation that taurine deficient hearts develop systolic and diastolic defects related to reduced SR Ca(2+) ATPase activity, a change mediated in part by reduced phospholamban phosphorylation.

The ubiquitin-proteasome system and autophagy are defective in the taurine-deficient heart.

Taurine depletion leads to impaired mitochondrial function, as characterized by reduced ATP production and elevated superoxide generation. These defects can fundamentally alter cardiomyocyte function and if left unchanged can result in cell death. To protect against these stresses, cardiomyocytes possess quality control processes, such as the ubiquitin-proteasome system (UPS) and autophagy, which can rejuvenate cells through the degradation of damaged proteins and organelles. Hence, the present study tested the hypothesis that reactive oxygen species generated by damaged mitochondria initiates UPS and autophagy in the taurine-deficient heart. Using transgenic mice lacking the taurine transporter (TauTKO) as a model of taurine deficiency, it was shown that the levels of ubiquitinated protein were elevated, an effect associated with a decrease in ATP-dependent 26S ß5 proteasome activity. Treating the TauTKO mouse with the mitochondria-specific antioxidant, mitoTEMPO, largely abolished the increase in ubiquitinated protein content. The TauTKO heart was also associated with impaired autophagy, characterized by an increase in the initiator, Beclin-1, and autophagosome content, but a defect in the generation of active autophagolysosomes. Although mitoTEMPO treatment only restores the oxidative balance within the mitochondria, it appeared to completely disrupt the crosstalk between the damaged mitochondria and the quality control processes. Thus, mitochondrial oxidative stress is the main trigger initiating the quality control systems in the taurine-deficient heart. We conclude that the activation of the UPS and autophagy is another fundamental function of mitochondria.

Impact of taurine depletion on glucose control and insulin secretion in mice.

Taurine, an endogenous sulfur-containing amino acid, is found in millimolar concentrations in mammalian tissue, and its tissue content is altered by diet, disease and aging. The effectiveness of taurine administration against obesity and its related diseases, including type 2 diabetes, has been well documented. However, the impact of taurine depletion on glucose metabolism and fat deposition has not been elucidated. In this study, we investigated the effect of taurine depletion (in the taurine transporter (TauT) knockout mouse model) on blood glucose control and high fat diet-induced obesity. TauT-knockout (TauTKO) mice exhibited lower body weight and abdominal fat mass when maintained on normal chow than wild-type (WT) mice. Blood glucose disposal after an intraperitoneal glucose injection was faster in TauTKO mice than in WT mice despite lower serum insulin levels. Islet beta-cells (insulin positive area) were also decreased in TauTKO mice compared to WT mice. Meanwhile, overnutrition by high fat (60% fat)-diet could lead to obesity in TauTKO mice despite lower body weight under normal chow diet condition, indicating nutrition in normal diet is not enough for TauTKO mice to maintain body weight comparable to WT mice. In conclusion, taurine depletion causes enhanced glucose disposal despite lowering insulin levels and lower body weight, implying deterioration in tissue energy metabolism.

Effect of taurine on ischemia-reperfusion injury.

Taurine is an abundant ß-amino acid that regulates several events that dramatically influence the development of ischemia-reperfusion injury. One of these events is the extrusion of taurine and Na+ from the cell via the taurine/Na+ symport. The loss of Na+ during the ischemia-reperfusion insult limits the amount of available Na+ for Na+/Ca2+ exchange, an important process in the development of Ca2+ overload and the activation of the mitochondrial permeability transition, a key process in ischemia-reperfusion mediated cell death. Taurine also prevents excessive generation of reactive oxygen species by the respiratory chain, an event that also limits the activation of the MPT. Because taurine is an osmoregulator, changes in taurine concentration trigger "osmotic preconditioning," a process that activates an Akt-dependent cytoprotective signaling pathway that inhibits MPT pore formation. These effects of taurine have clinical implications, as experimental evidence reveals potential promise of taurine therapy in preventing cardiac damage during bypass surgery, heart transplantation and myocardial infarction. Moreover, severe loss of taurine from the heart during an ischemia-reperfusion insult may increase the risk of ventricular remodeling and development of heart failure.

Role of taurine in the pathologies of MELAS and MERRF.

Taurine is an abundant ß-amino acid that concentrates in the mitochondria, where it participates in the conjugation of tRNAs for leucine, lysine, glutamate and glutamine. The formation of 5-taurinomethyluridine-tRNA strengthens the interaction of the anticodon with the codon, thereby promoting the decoding of several codons, including those for AAG, UUG, CAG and GAG. By preventing these series of events, taurine deficiency appears to diminish the formation of 5-taurinomethyluridine and causes inefficient decoding for the mitochondrial codons of leucine, lysine, glutamate and glutamine. The resulting reduction in the biosynthesis of mitochondria-encoded proteins deprives the respiratory chain of subunits required for the assembly of respiratory chain complexes. Hence, taurine deficiency is associated with a reduction in oxygen consumption, an elevation in glycolysis and lactate production and a decline in ATP production. A similar sequence of events takes place in mitochondrial diseases MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes) and MERRF (myoclonic epilepsy and ragged-red fiber syndrome). In both diseases, mutations in their respective tRNAs interfere with the formation of 5-taurinomethyluridine in the wobble position. Hence, the taurine-deficient phenotype resembles the phenotypes of MELAS and MERRF.

Effect of taurine and potential interactions with caffeine on cardiovascular function.

The major impetus behind the rise in energy drink popularity among adults is their ability to heighten mental alertness, improve physical performance and supply energy. However, accompanying the exponential growth in energy drink usage have been recent case reports and analyses from the National Poison Data System, raising questions regarding the safety of energy drinks. Most of the safety concerns have centered on the effect of energy drinks on cardiovascular and central nervous system function. Although the effects of caffeine excess have been widely studied, little information is available on potential interactions between the other active ingredients of energy drinks and caffeine. One of the active ingredients often mentioned as a candidate for interactions with caffeine is the beta-amino acid, taurine. Although taurine is considered a conditionally essential nutrient for humans and is thought to play a key role in several human diseases, clinical studies evaluating the effects of taurine are limited. However, based on this review regarding possible interactions between caffeine and taurine, we conclude that taurine should neutralize several untoward effects of caffeine excess. In agreement with this conclusion, the European Union's Scientific Committee on Food published a report in March 2003 summarizing its investigation into potential interactions of the ingredients in energy drinks. At the cardiovascular level, they concluded that "if there are any interactions between caffeine and taurine, taurine might reduce the cardiovascular effects of caffeine." Although these interactions remain to be further examined in humans, the physiological functions of taurine appear to be inconsistent with the adverse cardiovascular symptoms associated with excessive consumption of caffeine-taurine containing beverages.

Taurine deficiency and MELAS are closely related syndromes.

MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes) is a mitochondrial disease caused by one or more mutations of tRNA(Leu(UUR)). These mutations reduce both the aminoacylation of tRNA(Leu(UUR)) and a posttranslational modification in the wobble position of tRNA(Leu(UUR)). Both changes result in reduced transcription of mitochondria-encoded proteins; however, reduced aminoacylation affects the decoding of both UUG and UUA while the wobble defect specifically diminishes UUG decoding. Because 12 out of the 13 mitochondria-encoded proteins are more dependent on UUA decoding than UUG decoding, the aminoacylation defect should have a more profound effect on protein synthesis than the wobble defect, which more specifically alters the expression of one mitochondria-encoded protein, ND6. Taurine serves as a substrate in the formation of 5-taurinomethyluridine-tRNA(Leu(UUR)); therefore, taurine deficiency should mimic 5-taurinomethyluridine-tRNA(Leu(UUR)) deficiency. Hence, the wobble hypothesis predicts that the symptoms of MELAS mimic those of taurine deficiency, provided that the dominant defect in MELAS is wobble modification deficiency. On the other hand, if the aminoacylation defect dominates, significant differences should exist between taurine deficiency and MELAS. The present review tests this hypothesis by comparing the symptoms of MELAS and taurine deficiency.

Taurine as a marker for the identification of natural Calculus Bovis and its substitutes.

Calculus Bovis (C. Bovis) is a commonly used animal-derived therapeutic preparation. To meet the increasing clinical demand for the preparation, two artificial substitutes for Bos Taurus have been introduced in China: artificial C. Bovis and in vitro cultured C. Bovis. However, information on their efficacy and safety is inadequate. Therefore, we investigated the biological differences between the commonly used natural preparation and its two substitutes, with the aim of not only identifying the differences but also providing a procedure to distinguish between the different preparations.In the study, we prepared 9 natural C. Bovis, 2 artificial C. Bovis, and 2 in vitro cultured C. Bovis preparations for evaluation. Differences were noted between the three preparations relative to their effect on viability of cardiac fibroblasts from 1-day-old Wistar rats. Although natural C. Bovis had no effect on cell viability, 1-h treatment of the cells with 0.25 mg/ml of the substitutes significantly reduced cell viability, as detected by the MTS assay. Based on liquid chromatography and inductively coupled plasma mass spectrometry, the preparations also differed in composition. Indeed, the substitutes contained more taurine, cholic acid, iron, magnesium, and calcium than the natural preparations. They also differed spectroscopically.The present results reveal significant biological differences between natural C. Bovis and two of its substitutes. Since the substitutes appear to contain more taurine, cholic acid, and elements, these constituents may serve as markers to distinguish between natural C. Bovis and its substitutes.

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

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.