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 HCO 3 − -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 HCO 3 − -Cl − exchanger, platelet pH, and calcium concentration in essential hypertensive patients.

Recently, a C825T polymorphism in the gene coding for the beta3 subunit of G proteins (GNB3) has been described in cells from patients with essential hypertension and enhanced Na+/H+ exchange activity. This study aims to evaluate the association between the 825T allele and activity of erythrocyte sodium/lithium countertransport (Na+/Li+ CT) and other sodium transport systems in red blood cells from patients with essential hypertension. A group of 77 patients (36 male, 41 female; aged 51.7 +/- 1.1 years) was studied. The maximal rates (Vmax) of Na+/Li+ CT, Na+/K+/Cl- cotransport and Na+K+ ATPase were evaluated in erythrocytes from all the patients. They were genotyped for the C825T polymorphism by a polymerase chain reaction (PCR) method, followed by digestion with BseDI. Body mass index (BMI) was higher in CT+TT patients than in CC patients (28.9 +/- 0.5 vs. 27.0 +/- 0.7 kg/m2; P=0.023). Hypertensives with the T allele (CT+TT genotypes) showed significantly higher systolic blood pressure (BP) values (156.9 +/- 2.1 vs. 148.9 +/- 2.8 mmHg; P=0.024), whereas differences in diastolic BP did not reach statistical significance (96.4 +/- 1.0 vs. 94.0 +/- 1.1 mmHg; P=0.120). No differences in the Vmax of Na+/Li+ CT between the genotypes was seen (CC: 236 +/- 19 and CT+TT 277 +/- 23 mmol/L cells per h; P=0.221). Similarly, no differences were detected in the Vmax of erythrocyte Na+/K+/Cl- cotransport and Na+K+ ATPase among the genotypes. There was no appreciable association between the G-protein beta3-subunit C825T polymorphism and erythrocyte Na+/Li+ CT and other sodium transport systems in the hypertensive patient sample studied; however, those with the T allele were more obese and had more severe systolic hypertension.

Several sodium transport abnormalities have been reported in erythrocytes from essential hypertensive patients. The possible modification of these parameters under antihypertensive treatment remains controversial. We have measured the maximal rates of the Na+/K+ pump, Na+/K+/Cl- cotransport, and Na+/Li+ countertransport and the rate constant of Na+ leak in erythrocytes from 22 essential hypertensive patient responders to angiotensin converting enzyme inhibitors quinapril or captopril, and from 17 patient nonresponders to these drugs. In the former group, sodium transport measurements were performed at the baseline placebo period and after 6 months of active treatment. The maximal rate of Na+/Li+ countertransport decreased significantly after 6 months of treatment, without differences between both groups of treatment. Angiotensin converting enzyme inhibitors did not significantly modify other sodium transport parameters. The basal activity of erythrocyte sodium transport was not different between patients who responded or not to antihypertensive treatment with those drugs, excluding a predictive value of these measurements concerning the response to angiotensin converting enzyme inhibitors.

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