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Interaction between the actions of taurine and angiotensin II 总被引:1,自引:0,他引:1
Summary. 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, immundeficiency, 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.
Received November 10, 1998, Accepted May 19, 1999 相似文献
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Human transferrin. Expression and iron modulation of chimeric genes in transgenic mice 总被引:3,自引:0,他引:3
G S Adrian B H Bowman D C Herbert F J Weaker E K Adrian L K Robinson C A Walter C A Eddy R Riehl C J Pauerstein 《The Journal of biological chemistry》1990,265(22):13344-13350
Transferrin (TF) is a plasma protein that transports and is regulated by iron. The aim of this study was to characterize human TF gene sequences that respond in vivo to cellular signals affecting expression in various tissues and to iron administration. Chimeric genes were constructed containing 152, 622, and 1152 base pairs (bp) of the human TF5'-flanking region with the coding region of a reporter gene, CAT (chloramphenicol acetyltransferase), and introduced into the germ line of mice. Transgenes containing TF 5'-flanking sequences to -152 bp were expressed poorly in all tissues examined. In contrast, transgenes containing TF sequences to -622 or -1152 bp were expressed at high levels in brain and liver, greater than or equal to 1000-fold higher than tissues such as heart and testes. Liver and brain are major sites of endogenous TF mRNA synthesis, but liver mRNA levels are 10-fold higher than brain. A significant diminution of CAT enzymatic activity in liver accompanied iron administration in both TF(0.67) and TF(1.2)CAT transgenic mice, mimicking the decrease of transferrin in humans following iron overload. Levels of endogenous plasma transferrin also decreased in iron-treated transgenic mice. Transgenic mouse lines carrying human TF chimeric genes will be useful models for analyzing the regulation of human transferrin by iron and for determining the molecular basis of transferrin regulation throughout mammalian development into the aging process. 相似文献
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Genetic evidence that Neisseria gonorrhoeae produces specific receptors for transferrin and lactoferrin. 总被引:35,自引:10,他引:25
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K J Blanton G D Biswas J Tsai J Adams D W Dyer S M Davis G G Koch P K Sen P F Sparling 《Journal of bacteriology》1990,172(9):5225-5235
Transferrin (TF) and lactoferrin (LF) are probably the major sources of iron (Fe) for Neisseria gonorrhoeae in vivo. We isolated mutants of N. gonorrhoeae FA19 that were unable to grow with Fe bound to either TF (TF-) or LF (LF-) or to both TF and LF ([TF LF]-). The amount of Fe internalized by each of the mutants was reduced to background levels from the relevant iron source(s). The wild-type parent strain exhibited saturable specific binding of TF and LF; receptor activity was induced by Fe starvation. The TF(-)-specific or LF(-)-specific mutants were almost completely lacking in receptor activity for TF or LF, respectively, whereas the [TF LF]- mutants bound both TF and LF as well as the wild-type strain. All mutants utilized citrate and heme normally as Fe sources. These results demonstrate that ability to bind TF or LF is essential for gonococci to scavenge appreciable amounts of Fe from these sources in vitro. In addition, the TF and LF Fe acquisition pathways are linked by the mutual use of a nonreceptor gene product that is essential to Fe scavenging from both of these sources; this gene product is not required for Fe acquisition from other sources. 相似文献
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Megan E. Andriankaja Selahattin Danisman Lorin F. Mignolet-Spruyt Hannes Claeys Irina Kochanke Mattias Vermeersch Liesbeth De Milde Stefanie De Bodt Veronique Storme Aleksandra Skirycz Felix Maurer Petra Bauer Per Mühlenbock Frank Van Breusegem Gerco C. Angenent Richard G. H. Immink Dirk Inzé 《Plant molecular biology》2014,85(3):233-245
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Paths through the phytochrome network 总被引:3,自引:0,他引:3
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G M Shavlovsku E M Logvinenko D Schlee L V Koltun 《Biochimica et biophysica acta》1976,428(3):611-618
The effect of riboflavin and iron on 6-hydroxy-2,4,5-triaminopyrimidine synthesis rate was investigated in the cultures of the yeast Pichia guilliermondii (rib2 mutants) with the blocked second reaction to flavinogenesis. It was shown that riboflavin inhibited the 6-hydroxy-2,4,5-triaminopyrimidine synthesis rate in iron-rich and iron-deficient cells of mutants with low riboflavin requirements. Cycloheximide did not prevent the stimulation of 6-hydroxy-2,4,5-triaminopyrimidine synthesis caused by riboflavin starvation. 7-methyl-8-trifluoromethyl-10-(1'-D-ribityl)isoalloxazine strongly inhibited the 6-hydroxy-2,4,5-triaminopyrimidine synthesis, while 7-methyl-8-trifluoro-methyl-10-(beta-hydroxyethyl)izoalloxazine and galactoflavin exerted only a slight effect on this process. The 6-hydroxy-2,4,5-triaminopyrimidine synthesis rate in iron-deficient cells was significantly higher than in iron-rich cells. The 2,2'-dipyridyl treatment of iron-rich cells caused the stimulation of 6-hydroxy-2,4,5-triaminopyrimidine synthesis and cycloheximide abolished this effect. The results suggest that the activity of the first enzyme of flavinogenesis (guanylic cyclohydrolase) is under the control of feedback inhibition by flavins and the biosynthesis of this enzyme is regulated by iron. 相似文献
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