Literature DB >> 6311735

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.

J Duhm, B O Göbel, F X Beck.   

Abstract

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.

Entities:  

Mesh:

Substances:

Year:  1983        PMID: 6311735     DOI: 10.1161/01.hyp.5.5.642

Source DB:  PubMed          Journal:  Hypertension        ISSN: 0194-911X            Impact factor:   10.190


  5 in total

Review 1.  The Na-K-2Cl cotransport system.

Authors:  P Geck; E Heinz
Journal:  J Membr Biol       Date:  1986       Impact factor: 1.843

2.  Role of the furosemide-sensitive Na+/K+ transport system in determining the steady-state Na+ and K+ content and volume of human erythrocytes in vitro and in vivo.

Authors:  J Duhm; B O Göbel
Journal:  J Membr Biol       Date:  1984       Impact factor: 1.843

3.  Co-ordinated variations in chloride-dependent potassium transport and cell water in normal human erythrocytes.

Authors:  G W Stewart
Journal:  J Physiol       Date:  1988-07       Impact factor: 5.182

Review 4.  The regulatory function of mixed lineage kinase 3 in tumor and host immunity.

Authors:  Sandeep Kumar; Sunil Kumar Singh; Basabi Rana; Ajay Rana
Journal:  Pharmacol Ther       Date:  2020-10-09       Impact factor: 13.400

5.  Baseline Soluble Anti-erythropoietin Antibody Level Is an Independent Associated Factor for Follow-Up Erythropoietin Demand in Maintenance Dialysis Patients With End-Stage Renal Disease: A Prospective Cohort Study.

Authors:  Ying Zhang; Shi-Zhu Bian; Kun Yang; Yiqing Wang; Sha Tang; Weili Wang; Daihong Wang; Ling Nie; Jinghong Zhao
Journal:  Front Med (Lausanne)       Date:  2020-04-07
  5 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.