Partitioning of NaPi cotransporter in cholesterol-, sphingomyelin-, and glycosphingolipid-enriched membrane domains modulates NaPi protein diffusion, clustering, and activity. (33/127)

In dietary potassium deficiency there is a decrease in the transport activity of the type IIa sodium/phosphate cotransporter protein (NaPi) despite an increase in its apical membrane abundance. This novel posttranslational regulation of NaPi activity is mediated by the increased glycosphingolipid content of the potassium-deficient apical membrane. However, the mechanisms by which these lipids modulate NaPi activity have not been determined. We determined if in potassium deficiency NaPi is increasingly partitioned in cholesterol-, sphingomyelin-, and glycosphingolipid-enriched microdomains of the apical membrane and if the increased presence of NaPi in these microdomains modulates its activity. By using a detergent-free density gradient flotation technique, we found that 80% of the apical membrane NaPi partitions into the low density cholesterol-, sphingomyelin-, and GM1-enriched fractions characterized as "lipid raft" fractions. In potassium deficiency, a higher proportion of NaPi was localized in the lipid raft fractions. By combining fluorescence correlation spectroscopy and photon counting histogram methods for control and potassium-deficient apical membranes reconstituted into giant unilamellar vesicles, we showed a 2-fold decrease in lateral diffusion of NaPi protein and a greater than 2-fold increase in size of protein aggregates/clusters in potassium deficiency. Our results indicate that NaPi protein is localized in membrane microdomains, that in potassium deficiency a larger proportion of NaPi protein is present in these microdomains, and that NaPi lateral diffusion is slowed down and NaPi aggregation/clustering is increased in potassium deficiency, both of which could be associated with the decreased Na/Pi cotransport activity in potassium deficiency.  (+info)

Severe syncope and sudden death in children with inborn salt-losing hypokalaemic tubulopathies. (34/127)

BACKGROUND: Potassium deficiency may cause cardiac arrhythmias culminating in syncope or sudden death. METHODS: An inquiry performed among physicians caring for a total of 249 patients with inborn salt-losing tubulopathies revealed that acute cardiac complications occurred in seven children. RESULTS: Four patients died suddenly and three had severe syncope. These episodes occurred in the context of severe chronic hypokalaemia (< or =2.5 mmol/l) or were precipitated by acute diseases, which exacerbated hypokalaemia (< or =2.0 mmol/l). CONCLUSIONS: In conclusion, severe chronic or acute hypokalaemia is hazardous in inborn salt-losing tubulopathies.  (+info)

L1 cell adhesion molecule is neuroprotective of alcohol induced cell death. (35/127)

L1 cell adhesion molecule (L1), a protein critical for appropriate development of the central nervous system, is a target for ethanol teratogenicity. Ethanol inhibits both L1 mediated cell adhesion as well as L1 mediated neurite outgrowth. L1 has been shown to increase cell survival in cerebellar granule cells while ethanol has been shown to increase cell death. We sought to determine if L1 protected cells from ethanol induced cell death. Cerebellar granule cells from postnatal day 6 rat pups were cultured on either poly l-lysine with or without an L1 substratum. Alcohol was added at 2h post-plating and cell survival was measured at various times. L1 substratum significantly increased cell survival at 72 and 120 h. Ethanol significantly reduced cell survival at 48 h, with no effect at 72 or 120 h, both in the presence and absence of L1. At 48 h, L1 significantly increased cell survival in the presence of ethanol. We conclude that ethanol interferes with processes other than L1-L1 interactions in causing cell death, and that ethanol effects would be more severe in the absence of L1.  (+info)

Long-term aldosterone treatment induces decreased apical but increased basolateral expression of AQP2 in CCD of rat kidney. (36/127)

The purpose of the present studies was to determine the effects of high-dose aldosterone and dDAVP treatment on renal aquaporin-2 (AQP2) regulation and urinary concentration. Rats were treated for 6 days with either vehicle (CON; n = 8), dDAVP (0.5 ng/h, dDAVP, n = 10), aldosterone (Aldo, 150 microg/day, n = 10) or combined dDAVP and aldosterone treatment (dDAVP+Aldo, n = 10) and had free access to water with a fixed food intake. Aldosterone treatment induced hypokalemia, decreased urine osmolality, and increased the urine volume and water intake in ALDO compared with CON and dDAVP+Aldo compared with dDAVP. Immunohistochemistry and semiquantitative laser confocal microscopy revealed a distinct increase in basolateral domain AQP2 labeling in cortical collecting duct (CCD) principal cells and a reduction in apical domain labeling in Aldo compared with CON rats. Given the presence of hypokalemia in aldosterone-treated rats, we studied dietary-induced hypokalemia in rats, which also reduced apical AQP2 expression in the CCD but did not induce any increase in basolateral AQP2 expression in the CCD as observed with aldosterone treatment. The aldosterone-induced basolateral AQP2 expression in the CCD was thus independent of hypokalemia but was dependent on the presence of sodium and aldosterone. This redistribution was clearly blocked by mineralocorticoid receptor blockade. The increased basolateral expression of AQP2 induced by aldosterone may play a significant role in water metabolism in conditions with increased sodium reabsorption in the CCD.  (+info)

The effects of dietary potassium depletion on the ultrastructure of cardiac ventricular myocytes in rabbits: a morphometric study. (37/127)

The ultrastructure of cardiac ventricular myocytes isolated from normal and chronically K-depleted rabbits was analysed using morphometric techniques. Myocytes from normal animals showed a quantitatively similar distribution of organelle volumes to those previously reported for isolated myocytes from rat, and for whole myocardium in a variety of species. Myocytes from animals that had been fed a K-deficient diet for 25 days had a significantly increased surface density of junctional sarcoplasmic reticulum with the T-tubules and a significant increase in the surface density of the T-system itself. There were no other differences. The increase in junctional SR and T-system may be related to the defect in cardiac contractility that has been reported for rabbit following K depletion, and may represent an adaptive mechanism acting to protect the heart against Ca overload.  (+info)

Licking for taste solutions by potassium-deprived rats: specificity and mechanisms. (38/127)

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Acetazolamide prevents vacuolar myopathy in skeletal muscle of K(+) -depleted rats. (39/127)

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Calcium, magnesium, potassium and sodium intakes in Japanese children aged 3 to 5 years. (40/127)

The present study aimed to evaluate in preschool children the intakes of Ca, Mg that possibly affect health and tooth formation and the intakes of K and Na that may affect lifestyle-related diseases. Information on dietary intake was collected from 90 preschool children (15 boys and 15 girls each in the 3-, 4- and 5-year old groups) on 3 separate days in the school fiscal year 1999 (April 1999 to March 2000) by the duplicate-diet technique. The Ca, Mg, K, and Na concentrations were determined by atomic absorption spectrometry using wet-ashed samples. The medians of mean daily intakes of Ca, Mg, K and Na in 3- to 5-year-old children were 432 mg, 110 mg, 1.18 g and 1.60 g, respectively, and no significant differences with regard to gender were observed. Seasonal varia-tion of intake was seen for each mineral. Calcium intake in most preschool children did not meet adequate intake (AI), probably due to low intakes of milk and dairy products in Japan. Magnesium intake was below the estimated average requirement (EAR) in 13.3% of the subjects, while the K intake met the AI. Sodium intake in a quarter of preschool children exceeded the tentative dietary goal. We concluded that in Japanese children aged 3-5 years; Ca intake is low, Na intake is high, and K intake is adequate, but some children could be at risk for Mg deficiency.  (+info)