Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001127 (respiratory acidosis)
 1,501 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

DBcAMP or crystalline glucagon was utilized to elevate the intracellular cyclic AMP concentration in isolated rat hearts. Butyric acid, a metabolite of DBcAMP, was also investigated. Their effect on the intracellular pH (pHi) as determined by the distribution of [14C]DMO was investigated. Rat hearts, perfused with a recirculated modified Krebs-Henseleit solution maintained at 30 degrees C, were exposed to respiratory acidosis by bubbling the perfusate with 20% CO2. alpha- and beta-receptor antagonists were used to block the effects of endogenous catecholamines. Hypercapnia decreased the pHi from 7.09 to 6.82. A similar degree of hypercapnia decreased the pHi to only 6.95 in the presence of DBcAMP and to only 6.96 in the presence of glucagon. The effective buffer values (delta[HCO-3]i/deltapHi) were: control, 19; butyric acid, 16; DBcAMP, 139; glucagon, 148. These data suggest that cAMP mediates the effect of norepinephrine, which has been shown to diminish the change in pHi accompanying respiratory acidosis.
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PMID:The effect of dibutyryl cyclic AMP and glucagon on the myocardial cell pH1. 2 69

The purpose of this study was to clarify the means by which lithium induced a greatly diminished phosphaturic response to parathyroid hormone (PTH). Acutely thyroparathyroidectomized lithium-treated rats did not respond to PTH whereas similarly prepared animals in the presence of metabolic or respiratory acidosis exhibited a large phosphaturic response. Respiratory alkalosis significantly decreased fractional phosphate excretion and blocked the phosphaturic effect of PTH whereas PTH induced increases in cyclic AMP excretion in these animals. Lithium increased urinary excretion of oxoglutarate and citrate. In metabolic acidosis the restoration of PTH-dependent phosphaturia is accompanied by decreased organic acid excretion. No significant decrease of urinary citrate and oxoglutarate excretion occurred in respiratory acidosis in lithium-treated rats. It is suggested that PTH-dependent phosphate transport is mediated by intracellular pH but the increased excretion of citrate and oxoglutarate may reflect high intracellular levels of bicarbonate.
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PMID:Restoration of the phosphaturic effect of parathyroid hormone in lithium-treated rats. 61 80

Acute lithium administration (5 mmol/kg b.w.) to parathyroidectomized (PTX) rats induces extracellular acidosis, lower plasma phosphate concentration and increased phosphate reabsorption. The present studies evaluate the effect of lithium administration on tissue phosphate distribution, metabolites content in the kidneys and renal phosphate, 2-oxoglutarate and citrate transport in the presence and absence of db-cyclic AMP. Lithium decreased plasma and renal phosphate concentrations and increased phosphate concentration in the skeletal muscle, db-cyclic AMP was not phosphaturic in lithium-treated PTX rats. In PTX rats infused with 20 mM phosphate lithium depressed fractional phosphate excretion induced by db-cyclic AMP from 20 +/- 0.3% to 3.2 +/- 1.0%. However, metabolic or respiratory acidosis restored the responsiveness to db-cyclic AMP. Citraturia and ketoaciduria induced by lithium were depressed in db-cyclic AMP-treated rats. Kidney citrate and 2-oxoglutarate concentrations increased drastically, ATP level fell significantly whereas cAMP content did not change after lithium. We conclude that lithium administration increases phosphate uptake by the muscle which largely accounts for hypophosphatemia. The kidney responds with increased phosphate reabsorption independent of plasma and kidney phosphate concentrations, and with refractoriness to the phosphaturic effects of db-cyclic AMP. Acute lithium administration to rats induces extracellular acidosis and, probably, renal intracellular alkalosis as reflected by citraturia and ketoaciduria as well as the renal metabolite profile. The phosphaturic responsiveness to db-cyclic AMP is dependent, at least in part, on intracellular pH.
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PMID:Reversible resistance to the phosphaturic effect of db-cAMP in lithium-treated rats. 631 43