PMID: 9431846Feb 12, 1998Paper

Inhibition of furosemide-sensitive cation transport and activation of sodium-lithium exchange by endogenous circulating factor(s) in Bartter's and Gitelman's syndromes

Journal of Hypertension
L CalòAndrea Semplicini

Abstract

The nature of the cellular abnormality causing hypokalemia, hypotension, and hypovolemia in Bartter's and Gitelman's syndromes is still being debated. In fact, despite the recent descriptions of an array of nonconservative missense or point mutations in some ion transporters and in K+ channel, the lack of detectable defects in some patients suggests that other abnormalities of cell ion homeostasis may be involved in the pathophysiology of these syndromes. The study of the activity of cell ion transporters in patients with these syndromes using red blood cells (RBC) as a cellular model never investigated the role of plasma factor(s) affecting ion transport. To evaluate the effect of plasma from patients with these syndromes on furosemide-sensitive lithium efflux (FSLE) from lithium (Li+)-loaded RBC of healthy subjects in vitro. RBC of healthy controls were loaded with Li+ in the presence of nystatin and FSLE was evaluated in the presence of various concentrations of plasma from controls and patients with the two syndromes. Plasma from controls did not affect FSLE (0.08 +/- 0.02 mmol/l cells per h with 1:4 vol:vol and 0.07 +/- 0.02 mmol/l cells per h with 1:2 vol:vol plasma dilution). In contrast, doubling concentrations of plasm...Continue Reading

References

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Citations

Oct 22, 2002·Journal of Pharmacological and Toxicological Methods·Timothy C HardmanMark I M Noble
Feb 24, 2001·Critical Reviews in Clinical Laboratory Sciences·L CalòA Semplicini
Nov 14, 1998·Journal of Hypertension·M Alvarez-GuerraR P Garay
Dec 23, 1999·Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association·B DeliyskaI Tishkov
Oct 31, 1998·Journal of Hypertension·T Hardman, N N Chan

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