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Published on: March 14, 2017
Effects of acute hypercalcaemia on blood pressure in subjects with and without parathyroid hormone secretion
1Department of Medicine, University Hospital of North Norway, Tromsø, Norway. elena.kamycheva@unn.no
Insights
Acute hypercalcemia increases blood pressure, but the mechanism is unclear. A decrease in parathyroid hormone (PTH) secretion may contribute to this rise, suggesting PTH
Area of Science:
- Endocrinology
- Cardiovascular Physiology
Background:
- Acute hypercalcemia is known to elevate blood pressure.
- The precise mechanism behind this hypertensive effect remains uncertain.
- Parathyroid hormone (PTH) may influence blood pressure due to its vasodilatory properties, and its secretion decreases during hypercalcemia.
Purpose of the Study:
- To investigate the role of parathyroid hormone (PTH) secretion in the blood pressure response to acute hypercalcemia.
- To differentiate the effects of hypercalcemia from the effects of reduced PTH levels on blood pressure.
Main Methods:
- A calcium clamp technique was used to induce controlled hypercalcemia in two steps.
- The study included seven thyroparathyroidectomized subjects (with undetectable PTH) and ten control subjects.
- Subjects underwent both a calcium infusion and a placebo infusion on separate occasions.
Main Results:
- Systolic blood pressure significantly increased in control subjects during calcium infusion but not in thyroparathyroidectomized subjects.
- Serum PTH levels decreased promptly in controls during hypercalcemia.
- Hypercalcemia led to increased serum phosphate in both groups, but did not affect diastolic blood pressure, heart rate, or levels of catecholamines, renin, or aldosterone.
Conclusions:
- The blood pressure increase during acute hypercalcemia is not mediated by catecholamine secretion or the renin-aldosterone system.
- The observed fall in parathyroid hormone (PTH) secretion appears to play a contributory role in the hypertensive response to acute hypercalcemia.
Aim:
Acute hypercalcaemia increases the blood pressure, but the mechanism is uncertain. It may partly be the result of the concomitant fall in parathyroid hormone (PTH) secretion as PTH has been reported to have a vasodilator effect. To elucidate this, we infused calcium intravenously in subjects with and without PTH secretion.
Methods:
Seven thyroparathyroidectomized subjects with undetectable PTH levels and 10 controls were studied twice, once with a calcium clamp technique that increased plasma ionized calcium in two steps of 0.1 mmol L(-1), each step lasting 60 min, and once with a placebo infusion.
Results:
On the placebo day, blood pressure and all other variables were unaffected in both groups. On the calcium day, systolic blood pressure increased gradually and significantly from end of baseline till end of the calcium infusion in the controls (123.5 +/- 19.8 and 134.2 +/- 17.6 mmHg, P < 0.004) but not in the thyroparathyroidectomized subjects (124.9 +/- 15.7 and 126.0 +/- 20.6 mmHg, P = ns). Serum PTH levels fell promptly in the controls, and in both groups there was a significant increase in serum phosphate. The diastolic blood pressure and pulse rate, and the plasma adrenaline and noradrenaline, plasma renin activity, and serum aldosterone levels were unaffected by the calcium infusion.
Conclusion:
During acute hypercalcaemia the blood pressure increase appears unrelated to catecholamine secretion and the renin-aldosterone system, whereas the fall in PTH secretion may play a contributory role.
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