Isolated Kidney Cells Research Articles

Parathyroid hormone and phosphaturia

In conclusion, we have established that PTH inhibits H+ ion production in isolated kidney cells and in rat kidney slices. We presented evidence that this effect is due to an increased cellular concentration of cyclic AMP. These data strongly support our hypothesis that the phosphaturic effect of PTH is due to a depression of H+ secretion into the renal tubules which produces a rise in intraluminal pH. The rise in tubular fluid pH decreases the monovalent to divalent phosphate ratio. And since monovalent phosphate is at least 10 times more permeable than divalent phosphate, phosphate reabsorption is depressed and phosphate excretion increases.

The defect in insulin receptors in obese-hyperglycemic mice: A probable accompaniment of more generalized alterations in membrane glycoproteins

Although the liver plasma membranes of obese-hyperglycemic (ob/ob and db/db) mice bind less insulin than the membranes from thin litter mates, nearly equally depressed binding is observed for the general plasma membrane markers, concanavalin A and wheat germ agglutinin. Glucagon binding is virtually unchanged, and adenylate cyclase activity from obese mice is more sensitive to glucagon. Isolated kidney cells from obese mice have reduced insulin binding, but the decrease in WGA and con A binding is even more profound. Cultured (48 to 72 hours) spleen lymphocytes also have grossly reduced WGA and con A binding. The apparent change in insulin binding in obese animals may be but a minor part of generalized alterations in membrane glycoproteins. Factors complicating comparisons of hormone binding in different metabolic states are considered.

Treatment of Hypertensive Vascular Disease with Rice Diet

treatment of hypertensive vascular disease with the rice diet 1-5 was suggested by observations made on the protein, fat and carbohydrate metabolism of isolated kidney cells under various pathologic conditions (cell injury and/or changes in pH, sodium bicarbonate concentration, oxygen tension and metabolizable substrate 6-11 ). Until 1944 the consensus was that dietary treatment was useful in kidney disease but of no value in hypertensive vascular disease. The diet in uncomplicated hypertension requires no essential change from the normal. There is no justification for restriction of protein intake, indeed, such restriction may result in anemia and other evidences of malnutrition. Likewise, in the absence of edema or paroxysmal dyspnea, the restriction of salt is unwarranted; claims that such restriction may lower the blood pressure have not been substantiated. Obesity should be avoided for the same reasons that apply to normal individuals and not because of any demonstrated relationship to hypertensive

Kinetic analysis of calcium movements in cell culture. V. Intracellular calcium distribution in kidney cells.

The distribution of intracellular calcium was determined in isolated kidney cells by kinetic analyses of45Ca fluxes. Isotopic desaturation curves reveal an intracellular calcium compartment with a very slow time constant. The size of this calcium compartment is markedly increased by raising the extracellular calcium, by increasing the extracellular phosphate and may contain up to 99% of the intracellular exchangeable calcium. Accumulation of calcium in this pool is completely abolished by two specific inhibitors of mitochondrial calcium uptake, Antimycin A and Warfarin®. These results suggest that this compartment represents a pool of calcium in the cell mitochondria. The sudden removal of phosphate from the medium immediately stimulates calcium efflux from the cell. Conversely, an increase in medium phosphate immediately inhibits calcium efflux. Both effects are rapidly reversible. Finally, calcium efflux from the cells is stimulated after the cells are exposed to low temperature suggesting that calcium transport out of the cell may be regulated by the cytoplasmic calcium activity. These experiments are consistent with the view that mitochondria play an important role in the control and regulation of cytoplasmic calcium activity and of calcium transport.

Amino acid oxidase activity in renal glomeruli and tubular epithelial cells

The results of examinations of amino acid oxidase—known to form H 2O 2—in glomeruli and tubular epithelial kidney cells of rats and guinea pigs are reported. Twenty l-, dl-, and d-amino acids served as substrate. The amino acid activity, calculated as Qo 2 as well as the respiration, was clearly, but not always significantly higher in the glomerular cells of both species. The oxidation of the amino acids was found to be higher in the liver than in the total kidney homogenate, and partly even in the glomerular fraction. Further studies of the catalase in isolated kidney cells, decomposing the H 2O 2, even the portion formed by the amino acids, are under way.

The transport of inorganic ions and p-aminohippurate in isolated cells of the renal cortex of the rabbit

The transport of Na and K ions and of p-aminohippurate (PAH) was studied in isolated kidney cells of the rabbit. 1.1. During aerobic incubation at 25°, with 10 mM acetate as substrate there is active extrusion of Na+ from the cells and reaccumulation of K+. K+ accumulation from the medium into the cells is linearly dependent on the K+ concentration of the medium.2.2. Anaerobic incubation inhibits Na+ extrusion and water and K+ accumulation with a concomitant swelling of the cells. After oxygen is reintroduced, the cells again extrude Na+, reaccumulate K+ and the cell volume decreases.3.3. 10−4 M dinitrophenol has the same effect as anaerobiosis on the distribution of cations and water in isolated kidney-cortex cells.4.4. PAH was found to accumulate actively in isolated kidney cells. Cells that maintain their K+ content close to values found in fresh tissue during preparation in an optimal medium show the highest ability to accumulate PAH. At high K+ concentrations in the medium which increase the K+ cell content above normal, PAH accumulation is decreased.5.5. Increased Ca2+ concentration (7.5 mM) in the incubating medium decreases PAH accumulation by isolated kidney cells.6.6. The inhibitory effect of Li+ (20 mequiv/1) on PAH accumulation is partly reduced by increased Ca2+ concentrations in the medium; Ca2+ also changes the distribution of lithium between the cells and the medium.

Treatment of hypertensive vascular disease with rice diet

treatment of hypertensive vascular disease with the rice diet 1-5 was suggested by observations made on the protein, fat and carbohydrate metabolism of isolated kidney cells under various pathologic conditions (cell injury and/or changes in pH, sodium bicarbonate concentration, oxygen tension and metabolizable substrate 6-11 ). Until 1944 the consensus was that dietary treatment was useful in kidney disease but of no value in hypertensive vascular disease. The diet in uncomplicated hypertension requires no essential change from the normal. There is no justification for restriction of protein intake, indeed, such restriction may result in anemia and other evidences of malnutrition. Likewise, in the absence of edema or paroxysmal dyspnea, the restriction of salt is unwarranted; claims that such restriction may lower the blood pressure have not been substantiated. Obesity should be avoided for the same reasons that apply to normal individuals and not because of any demonstrated relationship to hypertensive