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J Duhm

Publications and source records attributed to J Duhm.

62 records · Page 4Linked to original sources

Sodium-lithium exchange and sodium-potassium cotransport in human erythrocytes. Part 1: Evaluation of a simple uptake test to assess the activity of the two transport systems.

A reliable and simple uptake test is proposed to assess the activity of the sodium lithium (Na+-Li+) countertransport and the sodium-potassium (Na+-K+) cotransport system of human erythrocytes. The test consists in measurement of phloretin-sensitive Li+ uptake from magnesium (Mg2+) media containing 2 mM Li+ and of furosemide-sensitive rubidium (Rb+) uptake from Na+ media containing 5 mM Rb+. Both Li+ and Rb+ are determined by atomic absorption spectrophotometry. The particular experimental conditions of the uptake assay are analyzed with respect to parameters that potentially affect the results, such as pH, cell volume, internal Na+, external Na+ and Rb+, presence of other ions, and concentration and protein-binding of furosemide, respectively. It is found that the activity of the two transport systems varies more than threefold among normotensive individuals, the activities in erythrocytes of each individual donor remaining stable within +/- 10% over more than two red cell life spans. The Li+ and Rb+ uptake rates are highly correlated to Li+ and K+ or Na+ release rates as determined by the methods of Canessa et al. and Garay et al. The test can thus be applied for routine screening in the search of "abnormalities" of red cell cation transport in hypertensive patients.

Biological Transport↗

Sodium-lithium exchange and sodium-potassium cotransport in human erythrocytes. Part 2: A simple uptake test applied to normotensive and essential hypertensive individuals.

The sodium-lithium (Na+-Li+) exchange and sodium-potassium (Na+-K+) cotransport activities were assessed on erythrocytes of 38 normotensive individuals, 18 patients with well-established essential hypertension, and five renal hypertensive patients, by means of an uptake assay method. With both transport systems, no significant differences in mean values and variance were observed among the three groups. Four of six low-renin essential hypertensive patients exhibited some of the lowest exchange and cotransport rates obtained among all individuals examined. The activity of both transport systems was slightly lower in women than in men.

Adult↗

Sodium and potassium ion transport accelerations in erythrocytes of DOC, DOC-salt, two-kidney, one clip, and spontaneously hypertensive rats. Role of hypokalemia and cell volume.

Sodium (Na+) and potassium (K+) transport by the furosemide-sensitive Na+-K+ transport system, the Na+-K+ pump, and the cation leak(s) were studied in erythrocytes from DOC-water, DOC-salt, two-kidney, one clip (Sprague-Dawley), and spontaneously hypertensive rats (Wistar-Kyoto). Rubidium (Rb+) was used as a tracer for K+. After 4 weeks of DOC-salt hypertension, inward K+ (Rb+) transport by the furosemide-sensitive system was increased threefold, and the inward Na+ leak and the red cell Na+ content were elevated by about 50%. The rise in cell Na+ accelerated K+ inward and Na+ outward transport by the Na+-K4 pump, DOC-water hypertension caused similar but less pronounced changes. In two-kidney, one clip hypertension, the Na+ leak and the Na+-K+ pump rates were slightly elevated, and furosemide-sensitive Rb+ uptake tended to be increased. In spontaneously hypertensive rats, furosemide-sensitive Rb+ uptake was accelerated by 50%. The marked hypokalemia in DOC-water and DOC-salt hypertension was associated with a slight loss of red cell K+ and an increase in mean cellular hemoglobin content (MCHC), indicative of cell shrinkage. Hypokalemia induced by dietary K+ deficiency caused alterations in red cell cation transport, content, and cell volume which were qualitatively similar but more pronounced than those seen in DOC-salt hypertension. Osmotic shrinkage in vitro induced a severalfold acceleration of furosemide-sensitive Rb+ uptake, similar to that observed in rat erythrocytes shrunken in vivo in K+-deficient states. It is concluded that the acceleration of furosemide-sensitive K+ (Rb+) transport in erythrocytes of mineralocorticoid hypertensive rats is largely caused by the hypokalemia and consecutive red cell K+ loss and shrinkage, respectively. Mean cellular hemoglobin content (MCHC) is thus a parameter that must be considered in studies on Na+ and K+ transport across the membrane of rat erythrocytes.

Animals↗