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Biomedical subjects

A B Borle

Publications and source records attributed to A B Borle.

12 recordsLinked to original sources
PubMed1979

Effect of pH on the calcium metabolism of isolated rat kidney cells.

The effects of metabolic and respiratory acidosis and alkalosis on cellular calcium metabolism were studied in rat kidney cells dispersed with collagenase. In both types of acidosis, the intracellular pH, total cell calcium, and the cell relative radioactivity after 60 min of labeling are significantly depressed. Kinetic analysis of 45-ca desaturation curves shows that acidosis decreases all three cellular calcium pools and depresses calcium fluxes between the superficial and cytosolic pools and between the cytosolic and mitochondrial pools. In alkalosis the intracellular pH, the total cell calcium, and the cell relative radioactivity are significantly increased. Kinetic studies show that in alkalosis, only the mitochondrial pool is consistently increased. Calcium exchange between the mitochondrial and cytosolic pool is increased in metabolic alkalosis only. These results suggest that hydrogen ion is an important modulator of calcium metabolism, and that the intracellular pH rather than extracellular pH is the critical factor in determining the calcium status of cells during altered acid-base conditions.

Acidosis↗
PubMed1979

Effects of adenosine 3',5'-monophosphate, dibutyryl adenosine 3',5'-monophosphate, aminophylline, and imidazole on renal cellular calcium metabolism.

The effects of cAMP, dibutyryl cAMP (DBcAMP), aminophylline, and imidazole on total cell calcium, calcium transport, and distribution were studied in cultured kidney cells by kinetic analysis of 45Ca uptake and desaturation curves. Low concentrations of the cyclic nucleotides (10(-7) and 10(-5) M) increase the total cell calcium, all intracellular exchangeable pools, and calcium transport between all cellular compartments. Aminophylline (1 mM) has effects qualitatively similar to cAMP and DBcAMP, while imidazole has opposite effects. At concentrations of 15 and 40 mM, imidazole depresses the total cell calcium and the cellular exchangeable calcium. Compared to the effects of parathyroid hormone (PTH), the changes obtained with 10(-7) and 10(-5) M cAMP are relatively modest, but higher concentrations (10(-3) M) of both cAMP and DBcAMP produce stimulations as marked as with 15 ng/ml PTH. The most dramatic changes are seen in the mitochondrial calcium pool and in the mitochondrial calcium exchange, which increase between 20- and 40-fold. These experiments show that cAMP mimics the effect of PTH on kidney cells and support the theory that cAMP is the mediator of PTH action on renal cell calcium transport.

Aminophylline↗
PubMed1978

Effects of calcium ionophores on the transport and distribution of calcium in isolated cells and in liver and kidney slices.

The effects of calcium ionophores on cellular calcium metabolism were studied in cultured kidney cells, in cells freshly isolated from rat kidney, and in liver and kidney slices. In isolated cells, these ionophores decreased the total cellular Ca content and the mitochondrial Ca. 45Ca efflux from prelabelled cells was also stimulated even in the absence of extracellular Ca. In slices, the ionphore A23187 increased the total slice Ca and the uptake of 45Ca. However, the mitochondria isolated from these slices treated with the ionophore had a lower total Ca and a depressed relative radioactivity. These results suggest that the increased cytosolic Ca produced by Ca ionophores may be due to mobilization of intracellular Ca stores rather than to a net shift of Ca from the extracellular fluids to the cell.

Animals↗
PubMed1978

Kinetic analysis of calcium desaturation curves from isolated kidney cells.

This paper provides mathematical solutions for calculating calcium fluxes and compartments in isolated kidney cells from calcium-45 desaturation curves. In contrast to other available methods, these solutions allow the calculation of kinetic parameters even if isotopic equilibrium has not been reached at the beginning of the desaturation period. To test the validity of the method, calcium-45 desaturation experiments were performed in isolated kidney cells after labeling periods of 30, 60, 90, or 120 min. Even though the calcium-45 desaturation curves differ with different labeling times, the respective values of the calculated parameters are practically identical. The optical labeling period was found to lie between 60 and 120 min. Since this new method does not require initial isotopic steady state, it allows a formal kinetic analysis of tracer desaturation curves even after short periods of labeling.

Biological Transport, Active↗
PubMed1978

Studies of calcium-45 desaturation from kidney slices in flow-through chambers.

This paper describes a method to measure calcium fluxes and calcium exchangeable pools in tissue slices by continuous perifusion in flow-through chambers. 45Ca desaturation from rat kidney slices can be analyzed as in an open three-compartment catenary system. A set of equations is given to calculate all the relevant kinetic parameters from the triple exponential equations which best fit the desaturation curves. The results show that the kinetic parameters obtained in kidney slices by this new method are in the same order of magnitude as those previously observed in cultured monkey kidney cells.

Animals↗
PubMed1978

Effects of parathyroid hormone on the distribution and transport of calcium in cultured kidney cells.

The effects of parathyroid hormone (PTH) on the transport and distribution of calcium in isolated kidney cells were studied by kinetic analysis of 45Ca desaturation curves. The results show that PTH (15 ng/ml) increases the total cell calcium content, every exchangeable pool, and all exchange rates. The greatest effect is observed in the slowest kinetic phase which reflects a mitochondrial pool. The effects of PTH occur even in the absence of magnesium and of phosphate and the larger effect is again obtained in the mitochondrial pool. These results suggest that PTH stimulates calcium transport in kidney cells by affecting the intracellular distribution of calcium or by stimulating calcium influx.

Biological Transport, Active↗
PubMed1975

Regulation of cellular calcium metabolism and calcium transport by calcitonin.

Calcitonin was studied in isolated kidney cells and in isolated mitochondria. A concentration of 10 ng/ml of synthetic calcitonin increases the cellular accumulation of 45Ca and the total cell calcium. The mitochondrial pool is increased several-fold. Kinetic analysis of the data shows that although the total cellular exchangeable calcium pool is enlarged, calcium influx and efflux are significantly depressed by calcitonin. The absence of phosphate or the presence of inhibitors of mitochondrial calcium transport completely abolish the effects of the hormone. In isolated mitochondria, the hormone stimulates the active calcium uptake and depresses the extramitochondrial calcium activity. Calcitonin counteracts the effects of cyclic AMP which stimulates the release of calcium from mitochondria and increases the extramitochondrial calcium activity. These data indicate that cellular calcium homeostasis is controlled by the mitochondrial calcium turnover. They suggest that calcitomin regulates the cell calcium metabolism and inhibits the transcellular calcium transport by stimulating the rate of calcium uptake by mitochondria which depresses cytoplasmic calcium activity.

Animals↗