Mechanism of acute hypercalcemic hypertension in the conscious rat

Tomas Berl, Moshe Levi, Marilyn Ellis, Cidio Chaimovitz

Research output: Contribution to journalArticlepeer-review

14 Scopus citations

Abstract

Acute hypercalcemia in the conscious, unanesthetized rat, achieved by a 30-minute infusion of CaCl2 (serum calcium level, 12.8 ± 0.6 mg/dl) resulted in significant elevation of mean arterial pressure (from 112 ± 2 mm Hg to 129 ± 3 mm Hg, p < 0.001). This pressor response was associated with a significant increase in systemic vascular resistance, from 0.45 ± 0.02 mm Hg/(ml/min)/kg body weight to 0.50 ± 0.02 mm Hg/(ml/min)/kg body weight (p < 0.05), but it caused no alteration in cardiac index. The pressor response to acute hypercalcemia does not appear to be mediated by vasopressor hormones or attenuated by vasodepressor hormones since inhibition of the renin-angiotensin system (nephrectomy), catecholamines (central and peripheral 6-hydroxydopamine), vasopressin (vascular antagonist), prostaglandins (indomethacin), and parathyroid hormone (parathyroidectomy) did not significantly alter the pressor response to infusion of CaCI2 in spite of similar serum calcium levels in all groups of animals. Rather, the pressor response to acute hypercalcemia seems to be mediated by a direct action of calcium ion on smooth muscle and perhaps myocardial cell contractility, since pretreatment with the calcium channel blockers verapamil or nifedipine blocked the pressor response to acute hypercalcemia.

Original languageEnglish
Pages (from-to)923-930
Number of pages8
JournalDimensions of Critical Care Nursing
Volume7
Issue number6
DOIs
StatePublished - 1 Jan 1985
Externally publishedYes

Keywords

  • Acute hypercalcemia
  • Calcium blockers
  • Hypertension mechanism

ASJC Scopus subject areas

  • Emergency
  • Critical Care

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