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 language | English |
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Pages (from-to) | 923-930 |
Number of pages | 8 |
Journal | Dimensions of Critical Care Nursing |
Volume | 7 |
Issue number | 6 |
DOIs | |
State | Published - 1 Jan 1985 |
Externally published | Yes |
Keywords
- Acute hypercalcemia
- Calcium blockers
- Hypertension mechanism
ASJC Scopus subject areas
- Emergency
- Critical Care