Beneficial effect of taurine in rabbits with chronic congestive heart failure

Takihara, Keiko; Azuma, Junichi; Awata, Nobuhisa; Ohta, Hikoto; Hamaguchi, Takashi; Sawamura, Akihiko; Tanaka, Yuya; Kishimoto, Susumu; Sperelakis, Nick

doi:10.1016/0002-8703(86)90360-1

Cited by 96 publications

(24 citation statements)

References 19 publications

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“…Since taurine exerts a modest positive inotropic effect in the hemodynamically depressed heart (Schaffer and Azuma, 1992), it has been proposed that taurine therapy benefits patients with heart failure by improving contractile function. This conclusion is supported by evidence that dP/dt is elevated in taurine-treated animals suffering from congestive heart failure (Takihara et al, 1986;Awata et al, 1987).…”

Section: Effect Of Taurine On Myocardial Contractility and Calcium Momentioning

confidence: 70%

Interaction between the actions of taurine and angiotensin II

2000

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The amino acid, taurine, is an important nutrient found in very high concentration in excitable tissue. Cellular depletion of taurine has been linked to developmental defects, retinal damage, immunodeficiency, impaired cellular growth and the development of a cardiomyopathy. These findings have encouraged the use of taurine in infant formula, nutritional supplements and energy promoting drinks. Nonetheless, the use of taurine as a drug to treat specific diseases has been limited. One disease that responds favorably to taurine therapy is congestive heart failure. In this review, we discuss three mechanisms that might underlie the beneficial effect of taurine in heart failure. First, taurine promotes natriuresis and diuresis, presumably through its osmoregulatory activity in the kidney, its modulation of atrial natriuretic factor secretion and its putative regulation of vasopressin release. However, it remains to be determined whether taurine treatment promotes salt and water excretion in humans with heart failure. Second, taurine mediates a modest positive inotropic effect by regulating [Na+]i and Na+/Ca2+ exchanger flux. Although this effect of taurine has not been examined in human tissue, it is significant that it bypasses the major calcium transport defects found in the failing human heart. Third, taurine attenuates the actions of angiotensin II on Ca2+ transport, protein synthesis and angiotensin II signaling. Through this mechanism taurine would be expected to minimize many of the adverse actions of angiotensin II, including the induction of cardiac hypertrophy, volume overload and myocardial remodeling. Since the ACE inhibitors are the mainstay in the treatment of congestive heart failure, this action of taurine is probably very important.

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Section: Effect Of Taurine On Myocardial Contractility and Calcium Momentioning

confidence: 70%

Interaction between the actions of taurine and angiotensin II

2000

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“…It has also been found to increase survival in rabbits with aortic insufficiency [63] and to have a protective effect in the murine model of iron overload cardiomyopathy [64]. There is a paucity of studies examining taurine administration to patients with CHF.…”

Section: Taurine and The Regulation Of Intracellular Calciummentioning

confidence: 99%

The management of conditioned nutritional requirements in heart failure

2006

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Patients suffering from congestive heart failure exhibit impaired myocardial energy production, myocyte calcium overload and increased oxidative stress. Nutritional factors known to be important for myocardial energy production, calcium homeostasis and the reduction of oxidative stress, such as thiamine, riboflavin, pyridoxine, L-carnitine, coenzyme Q10, creatine and taurine are reduced in this patient population. Furthermore, deficiencies of taurine, carnitine, and thiamine are established primary causes of dilated cardiomyopathy. Studies in animals and limited trials in humans have shown that dietary replacement of some of these compounds in heart failure can significantly restore depleted levels and may result in improvement in myocardial structure and function as well as exercise capacity. Larger scale studies examining micronutrient depletion in heart failure patients, and the benefits of dietary replacement need to be performed. At the present time, it is our belief that these conditioned nutritional requirements, if unsatisfied, contribute to myocyte dysfunction and loss; thus, restoration of nutritional deficiencies should be part of the overall therapeutic strategy for patients with congestive heart failure.

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“…Experimental and clinical studies of congestive heart failure have shown improvements and reduced mortality with taurine treatment [86,87]. However, another study has shown that taurine depletion might provide cardioprotection from regional ischemia [88].…”

Section: Taurine and The Heartmentioning

confidence: 99%

The role of taurine in diabetes and the development of diabetic complications

Hansen

2001

Diabetes Metabolism Res

243

157

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The ubiquitously found beta-amino acid taurine has several physiological functions, e.g. in bile acid formation, as an osmolyte by cell volume regulation, in the heart, in the retina, in the formation of N-chlorotaurine by reaction with hypochlorous acid in leucocytes, and possibly for intracellular scavenging of carbonyl groups. Some animals, such as the cat and the C57BL/6 mouse, have disturbances in taurine homeostasis. The C57BL/6 mouse strain is widely used in diabetic and atherosclerotic animal models. In diabetes, the high extracellular levels of glucose disturb the cellular osmoregulation and sorbitol is formed intracellularly due to the intracellular polyol pathway, which is suspected to be one of the key processes in the development of diabetic late complications and associated cellular dysfunctions. Intracellular accumulation of sorbitol is most likely to cause depletion of other intracellular compounds including osmolytes such as myo-inositol and taurine. When considering the clinical complications in diabetes, several links can be established between altered taurine metabolism and the development of cellular dysfunctions in diabetes which cause the clinical complications observed in diabetes, e.g. retinopathy, neuropathy, nephropathy, cardiomyopathy, platelet aggregation, endothelial dysfunction and atherosclerosis. Possible therapeutic perspectives could be a supplementation with taurine and other osmolytes and low-molecular compounds, perhaps in a combinational therapy with aldose reductase inhibitors.

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Beneficial effect of taurine in rabbits with chronic congestive heart failure

Cited by 96 publications

References 19 publications

Interaction between the actions of taurine and angiotensin II

Interaction between the actions of taurine and angiotensin II

The management of conditioned nutritional requirements in heart failure

The role of taurine in diabetes and the development of diabetic complications

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