Effects of acute hypercalcaemia on blood pressure in subjects with and without parathyroid hormone secretion

E Kamycheva1, R Jorde, E Haug

  • 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.
Abstract

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