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L G Welt

Publications and source records attributed to L G Welt.

At least 37 records · Page 2Linked to original sources
PubMed1968

The influence of the parathyroid glands on the hypercalcemia of experimental magnesium depletion in the rat.

Magnesium-deficient rats develop significant hypercalcemia, hypophosphatemia, and hyperphosphaturia. These changes suggest a state of hyperparathyroidism. This study examines the regulation of parathyroid gland activity in magnesium-deficient rats. Magnesium deficiency was induced in intact and chronically parathyroidectomized animals by feeding them a diet free of this cation. Control animals were pair fed and treated identically except for the inclusion of magnesium in their gavage solution.Magnesium-deficient rats with intact parathyroid glands developed significant hypercalcemia and hypophosphatemia. In addition, the concentration of ionic calcium in plasma was significantly elevated. In contrast, magnesium-deficient parathyroidectomized animals did not have a higher level of calcium in plasma than their nondeficient controls; they developed a decreased concentration of ionic calcium in the absence of a difference in the concentration of phosphate in plasma when compared with appropriate controls. The increased urinary excretion of phosphate was independent of the parathyriod status of the animals.It can be concluded that the hypercalcemia and hypophosphatemia of magnesium deficiency demands parathyroid gland activity and that the regulation of this activity is modified in the magnesium-deficient state to permit the maintenance of an elevated concentration of ionic calcium in plasma. Additional explanations must be found for the hyperphosphaturia.

Journal Article↗
PubMed1968

Concentration dependence of active potassium transport in the human red blood cell in the presence of inhibitors.

The active potassium influx in the human red blood cell is inhibited by strophanthidin, ethacrynic acid, and MK-870 (a new diuretic), and the degree of inhibition is greater at low concentrations of extracellular potassium than at high. In the case of ethacrynic acid, potassium appears to diminish the rate of combination of the drug with the transport system. The kinetic behavior of the active potassium influx in the presence of the inhibitors strophanthidin and ethacrynic acid is consistent with a model in which the binding of potassium at one of the potassium-sensitive sites in the transport system reduces the affinity of the system for the drug, and binding of a second potassium ion further reduces the affinity. It is not possible to distinguish between the sites on the basis of the studies presented here.

Biological Transport, Active↗
PubMed1967

The concentration dependence of active potassium transport in the human red blood cell.

The relation between the active potassium influx in the human red blood cell and the extracellular potassium concentration does not appear to be consistent with the Michaelis-Menten model, but is adequately described by a model in which two potassium ions are required simultaneously at some site or sites in the transport mechanism before transport occurs. The same type of relation appears to exist between that portion of the sodium outflux that requires the presence of extracellular potassium and the extracellular potassium concentration. Rubidium, cesium, and lithium, which are apparently transported by the same system that transports potassium, stimulate the potassium influx when both potassium and the second ion are present at low concentrations, as is predicted by the two-site model.

Biological Transport↗
PubMed1967

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Automation↗
PubMed1966

The renal lesions of electrolyte imbalance. IV. The intranephronic calculosis of experimental magnesium depletion.

A dietary depletion of magnesium in rats leads to the production in the thin limb of Henle's loop of the nephrons of spherical microliths composed of a matrix of PAS-positive substances and calcium phosphate (3). These microliths grow by accretion to form intranephronic calculi. The classical pathological syndrome of clinical nephrolithiasis is thus reproduced within the nephron; to wit, the origin of the calculus at a certain level, local traumatic damage at the site of its origin, passage with the fluid flow down the urinary passages, lodgment of the calculus at some restricting point, obstruction of fluid flow and the usual consequent localized intrarenal "hydronephrotic" alterations of regressive atrophic cellular dysplasias within the nephron. To the classical description of the two forms of urinary lithiases occurring in the bladder and in the renal pelvis must therefore be added a third form, intranephronic calculosis. From the first origin of a microlith to its ultimate form as a calculus its organized structure is characterized by its matrix (PAS-positive materials) in which the periodic precipitation of crystalline mineral (Ca(++), PO(3) (---)) occurs in a pattern simulating Liesegang rings.

Animals↗