Effects of Acute Mild Hypercalcemia or of the Calcium Antagonist Nifedipine on Cardiovascular Responsiveness to Norepinephrine or Angiotensin II in Normal Humans

Pressor doses of infused norepinephrine (NE) (mean pressure, +20 mm Hg) or angiotensin II (AII) (diastolic pressure, +20 mm Hg) and corresponding blood levels of NE or AII were assessed in 12 young normal subjects under basal conditions (study A), during slow calcium infusion (0.034 mg/kg/min) started 60 min previously (study C), and following 2 weeks of treatment with the Ca antagonist nifedipine, 50 mg/day (study D). Control values of blood pressure, 24-h urinary sodium, plasma NE, epinephrine, AII, and renin activity did not differ among the three studies. Plasma Ca was higher during study C than during studies A and D [10.7 +/- 0.8 (+/- SD) versus 9.1 +/- 0.3 mg/dl; p less than 0.01]. Plasma NE or AII levels obtained during NE or AII infusion as well as the pressor doses of AII were not modified by concomitant Ca infusion or following nifedipine. However, compared with basal conditions, the NE pressor dose tended to be decreased slightly during Ca infusion (106 +/- 71 versus 77 +/- 38 ng/kg/min; difference not significant) and was increased markedly following nifedipine (178 +/- 87 ng/kg/min; p less than 0.05). A control infusion of Ca alone (study B) during 120 min did not modify blood pressure or plasma renin and NE levels. Our observations suggest that in normal humans, inhibition of cellular Ca transport may predominantly affect the noradrenergic control mechanism, whereas angiotensinogenic cardiovascular regulation may be less dependent.