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Altered extracellular calcium homoeostasis in essential hypertension: a consequence of abnormal cell calcium handling
Insights
Hypertensive individuals show altered calcium metabolism, clearing exogenous calcium faster from circulation due to increased tissue uptake, not just kidney excretion. This suggests intracellular calcium handling differences in hypertension.
Area of Science:
- Cardiovascular Physiology
- Renal Physiology
- Cellular Metabolism
Background:
- Arterial hypertension is associated with calcium handling abnormalities.
- Previous studies indicate increased urinary calcium excretion and altered intracellular calcium in hypertension.
Purpose of the Study:
- To investigate exogenous calcium load handling in hypertensive vs. normotensive subjects.
- To identify differences in tissue calcium metabolism in vivo.
Main Methods:
- Intravenous calcium infusion (0.2 mmol/h/kg) in participants.
- Monitoring serum calcium levels during and after infusion.
- Evaluating urinary calcium excretion in timed collections.
Main Results:
- Hypertensive subjects exhibited lower serum ionized calcium levels throughout the study.
- Total body calcium clearance was significantly enhanced in hypertensive patients (P < 0.03).
- Renal calcium excretion was higher, but accounted for a minor fraction of total body clearance.
Conclusions:
- Hypertensive subjects demonstrate faster calcium disappearance from circulation.
- Enhanced total body calcium clearance is primarily due to increased tissue calcium uptake.
- Findings suggest altered cellular calcium handling in arterial hypertension.
Abstract:
A number of abnormalities in the extracellular and intracellular handling of calcium in arterial hypertension, namely an increased urinary calcium excretion, a reduced serum ionized calcium level and an enhanced intracellular free calcium concentration, have previously been reported by this and other laboratories. The present study aimed to investigate the handling of an exogenous calcium load in hypertensive and normotensive subjects in order to detect possible differences with regard to tissue calcium metabolism in vivo. A constant rate intravenous calcium infusion (0.2 mmol 2 h-1 kg-1 body wt.) was carried out in the participants. Serum calcium concentrations were determined at regular intervals during the infusion and in the 4 h after the end of the calcium load. Over the same period, urinary calcium excretion was evaluated in timed urine collections. Hypertensive subjects had lower serum ionized calcium levels compared with normotensive subjects at all the experimental points, a finding suggestive of a faster disappearance of calcium from the circulation. The total body calcium clearance, calculated from the area under the curve of the serum calcium concentrations, was enhanced in hypertensive patients (P less than 0.03). Although the renal calcium excretion was higher in hypertension, the renal calcium clearance accounted for only a minor fraction of the total body clearance, suggesting that the reduced serum calcium levels achieved by the hypertensive patients were not explained by the renal calcium leak. The enhanced total body calcium clearance found in hypertensive subjects is therefore due to an increased tissue calcium uptake. This finding provides indirect evidence of an altered cell calcium handling in hypertension.