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PubMed1999

[The effect of sodium alpha-glutarate on enzymatic transamination activity and on succinate dehydrogenase in rats with different resistances to hypoxia].

It have been found that intraperitoneal alpha-ketoglutarate injection (20 mg/100 g body weight) results in increase in the influence of cholinergic regulation mechanisms. It also results in increase of aminotransferase activity on background of the decrease of succinate dehydrogenase activity in liver and pancreas tissues and in small intestines mucous. Activity of transamination enzymes and succinate dehydrogenase activity is much higher in the case of rats with high hypoxia resistance, alpha-ketoglutarate injection results in increase of transamination enzymes activity in the organisms of rats with low resistance to hypoxia up to the control level of rats with high resistance, and simultaneously increases rats resistance to hypoxia. Effect of alpha-ketoglutarate injection on the energetical exchange in the tissues with different parasympathetic dependence taking from the animals with different hypoxia resistance is suppressed by blockade of M- and H-cholinoceptors.

Amination↗
PubMed1990

Sodium-coupled organic anion transport by Cancer borealis urinary bladder.

Recently, p-aminohippurate (PAH) transport by rat renal basolateral membrane (BLM) vesicles was shown to be coupled indirectly to the Na+ gradient through PAH-glutarate exchange and Na(+)-glutarate cotransport. We have examined the mechanism of PAH transport in Cancer borealis urinary bladder, a simple flat-sheet epithelium that is functionally analogous to vertebrate renal proximal tubule. These experiments indicate that crab bladder is capable of both Na(+)-coupled glutarate uptake and PAH-glutarate exchange and that PAH uptake may be coupled to Na+ in the intact tissue. First, glutarate uptake by intact bladder was lithium sensitive, Na(+) dependent, and inhibited by other dicarboxylates. In flux chambers, the bladder exhibited net glutarate secretion and tissue accumulation occurred primarily from the basolateral side. Furthermore, both BLM and brush-border membrane (BBM) vesicles also exhibited lithium-sensitive Na(+)-coupled glutarate uptake. Second, imposition of an in greater than out glutarate gradient markedly stimulated PAH uptake by bladder BLM vesicles, demonstrating PAH-glutarate exchange. In contrast, exchange was absent in BBM vesicles. Third, in intact bladder tissue, external glutarate increased the steady-state tissue-to-medium ratio for PAH from 14 +/- 1 to 19 +/- 1.5. This increase was both lithium inhibitable and Na+ dependent. Thus not only do bladder BLM show all the elements needed for indirect coupling of PAH transport to the Na+ gradient, but indirect coupling to Na+ can also drive uphill PAH transport in the intact epithelium.

Animals↗
PubMed1990

Rat renal cortical slices demonstrate p-aminohippurate/glutarate exchange and sodium/glutarate coupled p-aminohippurate transport.

In isolated basolateral membrane vesicles p-aminohippurate (PAH) transport may be coupled indirectly to the sodium gradient through PAH/glutarate [or alpha-ketoglutarate (alpha-KG)] exchange and Na/glutarate cotransport. In this study, rat renal cortical slices were used to examine indirect coupling of PAH transport to sodium in intact renal tissue. Like basolateral membrane vesicles, slices demonstrated avid uptake of 50 microM [14C]glutarate. Steady-state tissue/medium ratios of 30 were achieved by 90 to 120 min. Uptake was inhibited markedly by lithium and fumarate. PAH also inhibited glutarate accumulation, but through acceleration of glutarate efflux i.e., PAH/glutarate exchange, rather than direct inhibition of uptake. PAH-driven efflux of glutarate from slices was blocked by probenecid, which inhibits PAH/glutarate exchange in vesicles. Inasmuch as slices showed both Na/glutarate uptake and PAH/glutarate exchange, externally added glutarate should stimulate PAH uptake in slices. Indeed, in the presence of sodium, 50 microM external glutarate approximately doubled PAH accumulation by the slices. Stimulation by glutarate was abolished by either lithium or fumarate, or by elimination of sodium from the external buffer. The stimulatory effect was specific for glutarate or alpha-KG. Acetate, fumarate and succinate stimulated PAH uptake poorly, if at all. Neither fumarate nor lithium was able to eliminate concentrative PAH uptake completely, suggesting that a portion of PAH transport may occur without Na-dependent glutarate or alpha-KG recycling, i.e., that it may run directly off metabolic alpha-KG production or via a completely glutarate/alpha-KG independent mechanism.

Animals↗