Abstract
We evaluated the role of calcium metabolism on plasma noradrenaline concentration (pNA) and pressor response to infused noradrenaline (NA-R) in patients with mild-to-moderate essential hypertension (EHT). Mean arterial pressure (MAP), plasma ionized calcium (pCa2+), and NA-R were measured at the basal condition in 17 EHT and after the administration of calcium antagonist, nifedipine (60mg, t.i.d., for 4 weeks) in 9 EHT. Under basal condition, pCa2+ correlated positively with pNA and negatively with NA-R in EHT. Following nifedipine therapy, persistent reductions of MAP and NA-R, a transient increase in pNA and a sustained increase of urinary excretion of calcium were observed. On the other hand, no significant change in pCa2+ was found during the therapy. Percent change in MAP following 4 weeks of nifedipine administration correlated positively with pCa2+ and pNA before the therapy. In addition, change in NA-R by nifedipine therapy correlated positively with the basal values of pCa2+ and PNA and negatively with NA-R before the treatment. A significant negative correlation between NA-R and pNA was observed following nifedipine therapy as well as the basal state. However, the slope of the regression line between NA-R and pNA decreased significantly after the treatment as compared to the basal state. These results suggest that calcium metabolism relating sympathetic nerve activity and NA-R may contribute to the hypertensive mechanism in EHT. The hypotensive effects of nifedipine may be caused partly by the attenuation of sympathetic nerve activity and NA-R.
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