Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0003129 (Anoxia)
 551 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Proximal tubules (PSTs) of the S1, S2 and S3 segments and cortical collecting tubules (CCTs) were microdissected individually from rabbit kidneys and cultured for 7 days in hormonally defined media. Anoxia was induced by incubation of cultures in normal medium for 45 min at 25 degrees C in an atmosphere of nitrogen and cell death was measured by nigrosine dye uptake. After 45 min of anoxia and a 4- to 6-hr incubation in normal Ca++-containing media, cells from all segments were dead. Addition of calcium channel blockers verapamil and nifedipine (5 X 10(-7) and 10(-6) M, respectively) for the first 2 hr after anoxia to the incubation media was associated with a 60 +/- 8 and 33 +/- 7% survival of PST cells (5 hr after anoxia), p less than .05. Verapamil at 5 X 10(-8) M caused a 42 +/- 4% survival whereas nifedipine at 10(-7) M was not effective on the survival rate of PST cells (5 hr after anoxia). These calcium channel blockers also afforded protection from anoxic cell death for CCT cells. The role of calmodulin in anoxic cell injury was studied by means of calmodulin binding drugs, trifluoperazine and W7 [N-(6-aminohexyl)-5-chloronapthalene-sulfonamide]. Addition of trifluoperazine (5 X 10(-7) M) and W7 (5 X 10(-7) M to both PST and CCT cells during the 2-hr reflow period after 45 min of anoxia increased viability by 58 +/- 3 and 62 +/- 3%, respectively (P less than .05) at 5 hr postanoxia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Beneficial effects of calcium channel blockers and calmodulin binding drugs on in vitro renal cell anoxia. 372 95

The aim of this work was to study whether changes in fructose 2,6-bisphosphate concentration are correlated with variations of the glycolytic flux in the isolated working rat heart. Glycolysis was stimulated to different extents by increasing the concentration of glucose, increasing the workload, or by the addition of insulin. The glycolytic flux was measured by the rate of detritiation of [2-3H]- and [3-3H]glucose. Under all the conditions tested, an increase in fructose 2,6-bisphosphate content was observed. The glucose- or insulin-induced increase in fructose 2,6-bisphosphate content was related to an increase in the concentration of fructose 6-phosphate, the substrate of 6-phosphofructo-2-kinase. An increase in the workload correlated with a 50% decrease in the Km of 6-phosphofructo-2-kinase for fructose 6-phosphate. Similar changes in Km have been observed when purified heart 6-phosphofructo-2-kinase was phosphorylated in vitro by the cyclic AMP-dependent protein kinase or by the calcium/calmodulin-dependent protein kinase. Since the concentration of cyclic AMP was not affected by increasing the workload, it is possible that the change in Km of 6-phosphofructo-2-kinase, which was found in hearts submitted to a high load, resulted from phosphorylation by calcium/calmodulin protein kinase; other possibilities are not excluded. Anoxia decreased the external work developed by the heart, stimulated glycolysis and glycogenolysis, but did not increase fructose 2,6-bisphosphate.
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PMID:Role of fructose 2,6-bisphosphate in the control of heart glycolysis. 851 65