HYPERCALCEMIA ATTENUATES BLOOD-PRESSURE RESPONSE TO EPINEPHRINE

  • 1 December 1988
    • journal article
    • research article
    • Vol. 247  (3) , 949-952
Abstract
The potent alpha and beta adrenergic actions of epinephrine are probably mediated through an increase in free intracellular calcium concentration. Despite an absence of experimental evidence, many clinicans administer epinephrine with calcium to augment its cardiovascular effects. We evaluated the effects of calcium on epinephrine''s pressor response in both normal and endotoxin-treated rats by administering epinephrine to animals made hypercalcemic with calcium chloride or hypocalcenmic with the calcium chelator EGTA. EPI, given in incremental doses of 10, 20 and 50 .mu.g/kg, produced incremental increases in mean aterial pressure. Calcium chloride infused i.v. at a rate of 50 mg/ml hr significantly (P < .05) blunted (50% decrease) the hypertensive response to 50 .mu.g/kg epinephrine in normal animals. In endotoxin-treated rats, calcium chloride at 50 mg/ml/hr significantly blunted the hypertensive response to 10 .mu.g/kg (73% decrease), 20 .mu.g/kg (62% decrease) and 50 .mu.g/kg (50% decrease) epinephrine. Endotoxemia plus calcium chloride at 25 mg/ml/hr also significantly blunted (30% decrease) the hypertensive response to 50 .mu.g/kg EPI. By contrast, hypocalcemia produced by EGTA (30 mg/ml/hr) had no effect on epinephrine''s hypertensive effects in normal or endotoxemic rats. Since calcium chloride significantly diminishes epinephrine''s hypertensive effects in both normal and endotoxin-treated rats, the clinical use of calcium chloride along with epinephrine may not have a sound experimental basis.