Taurine heart muscle

If the heart is stressed sufficiently, cardie hypertrophy occurs (that is to say, the mass of the heart muscle increases) leading eventually to fibrosis and congestive heart failure. There is a doubling in taurine content in the affected ventricle in congestive heart failure in both man and animals. Except for a slight alteration in methionine content, the content of no other amino acid is altered (Peterson et al. 1973, Huxtable and Bressler 1974). 

Box 8.1 Taurine bile, brain, cats, heart, milk, sharks, shrimps and skeletal and cardiac muscle... 

Taurine (2-aminoethanesulfonic acid 4.235) is an inhibitory neurochemical that probably acts primarily as a neuromodulator rather than a neurotransmitter. It is formed from cysteine, and its accumulation can be prevented by the cardiac glycoside ouabain. Although receptor sites and specific actions cannot be elucidated without an antagonist, taurine has been implicated in epilepsy and, potentially, in heart disease. There are a large number of physiological effects attributed to taurine, among them cardiovascular (antiarrythmic), central (anticonvulsant, excitability modulation), muscle (membrane stabilizer), and reproductive (sperm motility factor) activity. Analogs of taurine, phthalimino-taurinamide (4.236) and its iV-alkyl derivatives, are less polar than taurine and are potent anticonvulsant molecules. 

Since Clenbuterol dilates blood vessels in skeletal muscle but relaxes smooth muscle blood vessels, the physical reactions are quite similar to the body s own epinephrine and can effect heart rate. It also reduces the level of the amino acid taurine in the heart which stabilizes cardiac rhythms, or the electrical activity in the heart. Increased intake for taurine during use was noted as wise. 

Outside the central nervous system, taurine in high concentrations is present in the heart, in striated muscle, in the adrenal gland, and in platelets and lymfocytes, but all tissues contain some taurine. 

In a first set of experiments we determined the production of taurine from hypotaurine, under the conditions previously described 7, in various tissues (brain, liver, kidney, spleen, heart, lung, muscle) of rats of different ages (5, 10, 18, 50, 120 days-old). The conclusions we could draw out from these observations were that in every case the enzymic activities... 

In order to characterize more closely the oxidation reaction of hypotaurine, we incubated homogenates of different tissues of adult mice with [ S]hypotaurine. These first incubations were carried out at 310 K and pH 7.4 for up to 4 h in open tubes without cofactors. We were unable for some time to convince ourselves whether or not there occurs any conversion of hypotaurine to taurine under such conditions. We continued tenaciously with our experiments, however, because hypotaurine was so rapidly converted to taurine in vivo. Only after numerous trials could we infer that there occurred some conversion also in vitro, but its detection was just at the sensitivity limits of our assay. It is thus no wonder that Cavallini et al. (1954) had earlier failed to detect any. Only 2-3% of the added hypotaurine were oxidized by homogenates of the liver and kidney, about 1% by the heart, spleen, muscle and lung, and still less by the brain. These traces of activity disappeared when the tissue samples were boiled or incubated at 273 K. The activity was slightly enhanced by NAD , NADP" " or oxidized glutathione, whereas reduced glutathione, NADH and NADPH had no effect. 

Administration of methoxamine, an a-agonist and vasoconstrictor, to rodents also produced a decrease in cardiac tissue and an increase in blood levels of taurine. On the other hand, taurine levels in the liver increased approximately 2.5- to 3-fold. While it is known that liver is capable of sequestering exogenous taurine, it can be calculated that the loss of taurine from the heart was quantitatively not sufficient to account for the increase in the liver. Thus the source of the increased taurine content of the liver is not known. Whether methoxamine stimulated de novo taurine synthesis in the liver or caused a loss of taurine from tissues other than the heart (such as skeletal muscle) which in turn was taken up by the liver requires further experimentation. 

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