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PubMed1973

Changes in kidney medullary phospholipid metabolism in the potassium-deficient rat. I.

Renal medullary phospholipids (PLs) increase rapidly in rats placed on a low potassium (K) diet. There is a unique pattern of morphologic change in renal medullary cells which parallels this biochemical alteration. Highly membranous multivesicular bodies (MVBs) appear in all cell types of the kidney medulla, and the number and size of these MVBs increase with further K depletion. Medullary PL levels are doubled in rats after 11 days on the low K diet and continued increase occurs with longer depletion. There are no major changes in the relative proportion of different medullary PL species with this increase. The rise in PL levels is quickly reversed by the addition of K to the low K diet of depleted rats. Potassium repletion returns renal medullary PL levels to normal values with a concomitant rapid loss of MVBs from medullary cells. Tissue slices of kidney medulla from rats in various stages of K depletion have been incubated with radioactive precursors of PL. These incubation studies indicate that the in vitro ability to incorporate label into PL is increased in medulla from K-depleted animals, suggesting that increased renal medullary PL synthesis causes the PL accumulation in K deficiency.

Animals↗
PubMed1980

Potassium deficiency enhances the effect of thyroid hormone on NaK-ATPase in liver and kidney.

In order to examine the possibility that the changes in electrolytes in tissue alter the effect of thyroid hormone on NaK-ATPase, rats were fed either synthetic K-deficient diet or synthetic K-normal diet. K-deficient diet induced a reduction in K content in serum or kidney, while that of the liver remained unchanged. When a daily dose of 2.5 micrograms T3 was administered for 7 days to k-deficient rats, both Mg- and NaK-ATPase of the homogenate of liver and kidney were elevated, while the same dose failed to influence those enzymes in K-normal rats. Furthermore, T3 dose increased the Na content of liver and kidney in K-deficient rats, resulting in a significant decrease in th K/Na ratio in those tissue. Based on the estimation from chloride space, the decrease in K/Na was deemed to have occurred mainly in the intracellular space. As the levels of serum thyroid hormone and liver T3 were not influenced by K-deficiency, the effect of K depletion is likely to be mediated not through the alteration in thyroid hormone kinetics, but through some other mechanism such as the elevation of intracellular Na. The present study demonstrates that K deficiency may sensitize NaK-ATPase to the effect of thyroid hormone.

Adenosine Triphosphatases↗
PubMed1993

[Myopathy due to potassium deficiency in eight cats and a dog].

Eight cats and one dog with signs of cervical ventroflexion, reluctance to walk, a stiff and stilted gait and muscle weakness are introduced. Though blood potassium concentration was very low (< 3.0 mval/l) in one cat and the dog only, a potassium depletion myopathy was assumed as the cause of these symptoms. Two of three cats had elevated values of the urinary fractional potassium excretion compared to ten healthy cats. Blood creatinine values were within normal ranges. Five of seven cats had elevated creatine kinase values. All animals improved after potassium substitution. Causes of potassium depletion are discussed and differential diagnoses of myopathies are briefly mentioned.

Animals↗