(Hypertension. 1996;27:456-464.)
© 1996 American Heart Association, Inc.
Articles |
From the Department of Chemistry, Loyola University of Chicago (Y.C., D.M. de F.), and the Renal Disease and Hypertension Section, Loyola University Stritch School of Medicine, Maywood (M.S., V.K.B.), Ill.
Abstract Enhanced Na+-Li+ exchange activity has been reported in red blood cells (RBCs) of white patients with essential hypertension compared with RBCs of normotensive individuals. To understand the factors responsible for this finding, we applied novel and conventional spectroscopic and kinetic methods to blood samples from 10 hypertensive and 10 normotensive individuals. We measured the kinetic parameters (Vstd, Vmax, and Km) for RBC Na+-Li+ exchange by atomic absorption spectrophotometry and used 23Na and 7Li nuclear magnetic resonance relaxation methods to measure Na+ and Li+ binding to RBC membranes as well as 31P nuclear magnetic resonance spectroscopy to measure membrane phospholipid compositions. We found significant differences between the two groups for the affinity of Na+ for the RBC membrane (0.202±0.054 mmol/L-1 for hypertensive patients versus 0.296±0.071 mmol/L-1 for normotensive subjects, P<.005). The kinetic parameters of RBC Na+-Li+ exchange (Vstd, Vmax, and Km) were 0.32±0.09 and 0.66±0.17 mmol Li+/L cell·h and 160±62 mmol/L, respectively, for hypertensive patients versus 0.21±0.06 and 0.32±0.14 mmol Li+/L cell·h and 86±69 mmol/L for normotensive subjects (P<.05). The fractions of phosphatidylserine and phosphatidylethanolamine were 0.153±0.009 and 0.294±0.016 for hypertensive patients versus 0.138±0.013 and 0.325±0.018 for normotensive subjects (P<.05). The Na+ binding constants were negatively correlated with the Km values for both the hypertensive (r=-.61, P=.01) and normotensive (r=-.43, P=.04) groups. Changes in lipid-protein interactions in the RBC membranes of hypertensive patients appear to be responsible for weaker Na+ binding to the membrane and for the faster rates of RBC Na+-Li+ exchange.
Key Words: hypertension, essential membranes erythrocytes ions nuclear magnetic resonance
This article has been cited by other articles:
![]() |
C. G. Savopoulos, A. I. Hatzitolios, N. A. Katsiki, M. Baltatzi, M. Kosmidou, N. Raikos, D. P. Mikhailidis, A. G. Ziakas, G. Kaiafa, and N. Tsesmeli Sodium-Lithium Countertransport Activity in Healthy, Dyslipidemic, and Hypertensive Individuals Angiology, January 1, 2009; 59(6): 727 - 735. [Abstract] [PDF] |
||||
![]() |
S. N. Orlov, N. C. Adragna, V. A. Adarichev, and P. Hamet Genetic and biochemical determinants of abnormal monovalent ion transport in primary hypertension Am J Physiol Cell Physiol, March 1, 1999; 276(3): C511 - C536. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Pahor, M. B. Elam, R. J. Garrison, S. B. Kritchevsky, and W. B. Applegate Emerging Noninvasive Biochemical Measures to Predict Cardiovascular Risk Arch Intern Med, February 8, 1999; 159(3): 237 - 245. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. Zicha, Z. Dobesova, and J. Kunes Plasma Triglycerides and Red Cell Ion Transport Alterations in Genetically Hypertensive Rats Hypertension, September 1, 1997; 30(3): 636 - 640. [Abstract] [Full Text] |
||||
|
Hypertension Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 1996 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |