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(Hypertension. 1996;27:919-925.)
© 1996 American Heart Association, Inc.

Articles

Erythrocyte Sodium Transport, Intraplatelet pH, and Calcium Concentration in Salt-Sensitive Hypertension

María del Mar Lluch; Alejandro de la Sierra; Esteban Poch; Antonio Coca; María Teresa Aguilera; Montserrat Compte; Alvaro Urbano-Márquez

From the Hypertension Unit, Departments of Internal Medicine and Nephrology (E.P.), Hospital Clínic, University of Barcelona (Spain).

Correspondence to Alejandro de la Sierra, MD, Department of Internal Medicine, Hospital Clínic, Villarroel 170, 08036-Barcelona, Spain.

Abstract We evaluated changes in erythrocyte sodium transport systems, platelet pH, and calcium concentration induced by low and high salt intakes in a group of 50 essential hypertensive patients classified on the basis of their salt sensitivity. Patients received a standard diet with 20 mmol NaCl daily for 2 weeks supplemented in a single-blind fashion by placebo tablets the first 7 days and NaCl tablets the following 7 days. Salt sensitivity, defined as a significant rise (P<.05) in 24-hour mean blood pressure obtained by ambulatory blood pressure monitoring, was diagnosed in 22 (44%) patients. The remaining 28 (56%) were considered to have salt-resistant hypertension. In the entire group of hypertensive patients, high salt intake promoted a significant increase (P<.05) in the maximal rate of erythrocyte Na⁺-Li⁺ countertransport (from 271±19 to 327±18 µmol/(L cells/h) and of the Na⁺-dependent HCO₃^--Cl^- exchanger (from 946±58 to 1237±92 µmol/L cells/h) as well as in platelet pH (from 7.15±0.01 to 7.19±0.02) and calcium concentration (from 49±2 to 57±2 nmol/L). Depending on salt sensitivity, high salt intake promoted opposing changes in some of the sodium transport systems studied. Salt-sensitive patients increased the maximal rate of the erythrocyte Na⁺-K⁺ pump (from 7.0±0.4 to 8.8±0.4 mmol/(L cells/h), Na⁺-K⁺-Cl^- cotransport (from 416±37 to 612±41 µmol/(L cells/h), and Na⁺-Li⁺ countertransport (from 248±20 to 389±17 µmol/(L cells/h) at the end of the high salt period. Conversely, salt-resistant patients decreased the Na⁺-K⁺ pump (from 8.0±0.4 to 6.9±0.3 mmol/(L cells/h) and Na⁺-K⁺-Cl^- cotransport (from 578±53 to 481±43 µmol/(L cells/h). We conclude that modulation of erythrocyte sodium transport systems by high salt intake depends on salt sensitivity. The Na⁺-K⁺ pump, Na⁺-K⁺-Cl^- cotransport, and Na⁺-Li⁺ countertransport increase in salt-sensitive patients, whereas the activity of these sodium transport systems tends to decrease in salt-resistant patients. Independent of salt sensitivity, high salt intake promotes a significant increase in the erythrocyte Na⁺-dependent HCO₃^--Cl^- exchanger, platelet pH, and calcium concentration in essential hypertensive patients.

Key Words: hypertension, sodium-dependent • sodium, dietary • ions • sodium-potassium pump • calcium

This article has been cited by other articles:

				E. Bragulat, Alejandro de la Sierra, M. T. Antonio, and A. Coca Endothelial Dysfunction in Salt-Sensitive Essential Hypertension Hypertension, February 1, 2001; 37(2): 444 - 448. [Abstract] [Full Text] [PDF]

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