Lluch Mm

Assessment of salt sensitivity in essential hypertension by 24-h ambulatory blood pressure monitoring

We used ambulatory blood pressure monitoring (ABPM) in the assessment of salt sensitivity in 40 essential hypertensive patients, comparing 24-h mean blood pressure during 7 days of low salt (20 mmol NaCl/day) and high salt (260 mmol NaCl/day) intake. Salt sensitivity was diagnosed in 18 essential hypertensive patients (45%), each of them showing a significant increase in mean blood pressure (P < .05) from low to high salt diet. Salt-sensitive patients exhibited a high-salt-dependent increase in all blood pressure parameters including 24-h systolic, mean, diastolic blood pressure, blood pressure load, area under the curve, and awake and asleep blood pressure values. These patients exhibited a nondipper profile on both low-salt and high-salt diets. Salt-resistant patients (55%) showed a decrease in awake, and an increase in asleep blood pressure values after high salt intake, thus tending to flatten the circadian blood pressure profile. We conclude that ABPM is a useful method to assess salt sensitivity. In salt-resistant patients high salt intake induces a significant increase in asleep blood pressure with no significant changes in 24-h blood pressure, promoting a flattened blood pressure curve and tending to transform a dipper into a nondipper profile, which could have important implications in end-organ damage.

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

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 microM/(L cells/h) and of the Na(+)-dependent HCO3(-)-CL(-) exchanger (from 946 +/- 58 to 1237 +/- 92 microM/L cells/h) as well as in platelet pH (from 7.15+/-0 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 (fom 7.0 +/- 0.4 to 8.8 +/- 0.4 mmol/(L cells/h), Na(+)-K(+)-Cl(-) cotransport (from 416 +/- 37 to 612 +/- 41 micromol/(L cells/h), Na(+)-Li(+) countertransport (from 248 +/- 20 to 389 +/- 17 micromol/(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 micromol/(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.

Comparative evaluation of the antihypertensive efficacy of once-daily amlodipine versus nitrendipine with 24-hour ambulatory blood pressure monitoring in essential hypertension.

Summary We compared the antihypertensive efficacy of once-daily amlodipine (AM) versus nitrendipine (NTR) by 24-h ambulatory blood pressure monitoring (24-h ABPM) in 32 patients with mild to moderate essential hypertension (EH). After a 2-week single-blind, placebo run-in period, patients were randomized in a double-blind, parallel fashion: 14 received AM 5 mg and 18 NTR 10 mg. After 2 weeks, dose was adjusted if necessary (AM 10 mg or NTR 20 mg) and continued for another 6-week period. At the end of the placebo period and during the last week of treatment, patients underwent 24-h ABPM. Initial office BP mean values were similar in both groups (169.8 ± 14/102.5 ± 6 vs. 167.1 ± 14/98.7 ± 5 mm Hg, respectively, p = NS). A comparable decrease in office mean values of systolic BP (SBP, −22.3 ± 13 vs. −19.1 ± 16 mm Hg) and diastolic BP (DBP, −12.0 ± 5 vs. −8.1 ±8 mm Hg) was observed. Nevertheless, 24-h ABPM mean values differed significantly between patients treated with AM or NTR with regard to 24-h SBP (120.0 ± 10 vs. 132.5 ± 1 mm Hg, p = 0.01). Moreover, the average decrease in 24-h SBP (-19.3 ± 6 vs. −5.2 ± 11 mm Hg, p = 0.0036) and 24-h DBP (-10.7 ± 4 vs. −3.7 ± 6 mm Hg, p = 0.0047) was higher in the AM group, with no changes in 24-h heart rate (HR). At equivalent once-daily dosage, AM was more effective than NTR in decreasing BP assessed by 24-h ABPM.

Detection of a circulating inhibitor of the Na+-K+-Cl− cotransport system in plasma and urine after high salt intake

The aim of the study was to detect the presence of an endogenous Na(+)-K(+)-Cl- cotransport inhibitor factor in plasma and urine from salt-loaded subjects. Twenty-six essential hypertensive patients (13 men, 13 women) and 6 normotensive controls (2 men, 4 women) received a diet containing 260 mmol/day of NaCl tablets for 7 days. Human erythrocytes from healthy blood donors (using bumetanide-stimulated Li+ efflux) were used to test the inhibition of Na(+)-K(+)-Cl- cotransport by different plasma and urine concentrations collected the last day of the salt-loaded period. The addition of plasma and urine from salt-loaded subjects significantly inhibited erythrocyte Na(+)-K(+)-Cl- cotransport (P < .001). No differences were observed between hypertensive patients and normotensive controls. These results provide evidence of an Na(+)-K(+)-Cl- cotransport inhibitor factor in plasma and urine from salt-loaded humans, in concordance with previous reports in salt-loaded rats.