• Nebojsa Tasić, Milica Nesović, Dragan Djurić, and Vladimir Kanjuh.
• Dedinje Institute of Cardiovascular Diseases, Belgrade. ntasa@Eunet.yu
• Srp Ark Celok Lek. 2002 Jan 1;130(1-2):7-12.

IntroductionIt has been reported that changes in salt loading influence parameters of calcium metabolism in hypertensive subjects. It was also reported that response of blood pressure to salt intake is related to salt-induced increase in intracellular calcium and decrease in intracellular magnesium concentrations [1]. Several authors showed that salt-sensitive hypertensive subjects significantly decreased blood pressure after calcium intake which was emphasized by high salt intake. Resnick et al. showed that during high salt intake regimen increase in blood pressure was followed with decrease in serum calcium level, this was explained by the fact that high salt intake stimulates the calcium uptake by cells [2]. They also reported the following characteristics of hypertensive patients with additionally lower blood pressure as a response to calcium intake: salt-sensitive, low serum ionized calcium and plasma renin activity (PRA) values and high parathyroid hormonE (PTH) values and 1.25-(OH)2-D values. The aim of the study was to evaluate values of corrected and ionized serum and urine calcium in a group of salt-sensitive patients, salt-resistant patients and a whole group during normal salt-intake regimen, and a group without salt and during sodium load (10 g salt extra).Material And MethodsIn our study, 50 untreated patients (27 women and 23 men; average age 42 +/- 9.2 yrs; average BMI 27.91 +/- 4.6 kg/m2) with essential hypertension were put on a high salt regimen (200 mmol NaCl per day) for one week after a week on a low salt diet (20 mmol NaCl per day). On the last day of the normal regimen and during the 1st, 3rd and 5th day of low salt and high salt regimens, the following follow-up was carried out: total (corrected) serum calcium level and total urine calcium level, ionized serum calcium urine creatininE level; serum albumin and daily diuresis and blood pressure. All patients had normal sodium and potassium serum concentrations. Salt intake was checked by taking a specimen of 24-hour urine considered as satisfactory if sodium excretion of 100 to 150 mmol/d (mmol per day) was noted. During the whole hospital examination, calcium intake through hospital meals was standardized to about 817 mg of calcium daily. Salt sensitivity was defined as 10 mmHg increase in mean blood pressure at the end of high vs. low salt diet. Salt sensitive group consisted of 26 patients and salt insensitive of 24 patients.ResultsAccording to sex, there was no statistically significant difference: 27 females (54%) and 24 males (46%). Average age of patients was 49 +/- 9.2 yrs, ranging from 21 to 64 with normal frequency distribution. Average body weight was 80.49 kg +/- 12.45 kg. Body height was from 150 to 192 cm with average of 170.12 +/- 10.53 cm. Average value of Body Mass Index (BMI in kg per square meter) was 27.91 +/- 4.6. In the studied patients average duration of hypertension was 6.98 +/- 6.4 yrs with non-homogeneous distribution. In 32 patients (64%) the medical history confirmed that one or more family members had hypertension. It was found that salt loading significantly decreased ionized calcium (F = 2.49; p < 0.05) and significantly increased urinary excretion of calcium (F = 5.22; p < 0.001) in salt sensitive patients in comparison with salt insensitive subjects. Serum calcium did not differ significantly during different salt intake regimens between two groups. Our study revealed no positive correlation between gender, age, BMI and family history and calcium metabolism.ConclusionThe findings of this study support the opinion of altered calcium metabolism in hypertensive subjects sensitive to salt intake. By demonstrated results we tried to define clinically different pathophysiologic and potentially different therapeutic subgroups in hypertensive population and to point to clinical and biochemical heterogeneity of primary hypertension.

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