Influences of different antihypertensive treatments on indices of systemic mineral metabolism

A negative calcium balance has previously been described in human hypertension with low levels of plasma ionized calcium (Ca2+) and an increased urinary excretion of calcium. The cause of this disturbance in mineral metabolism is not known, nor is it known if this derangement could be abolished if blood pressure is reduced by antihypertensive treatment. In the present investigation, the effects of antihypertensive monotherapy on serum and fasting urinary electrolytes were studied. For 3 to 6 months, 319 hypertensive patients entered 17 study groups, each group using one of the following antihypertensive drugs: dilevalol, metoprolol, antenolol, pindolol, propranolol, hydrochlorothiazide, bendrofluomethiazide, furosemide, spironolactone, doxazocine, prazocine, diltiazem, verapamil, nifedipine, isradipine, captopril, or lisinopril. Treatment with different beta-blockers, as well as diuretics, reduced the fasting urinary calcium excretion (P < .001). However, while the beta-blockers increased the proportion of the ionized form of calcium in blood (Ca2+) (P < .001), Ca2+ was further decreased by diuretic treatment (P < .05). Angiotensin converting enzyme inhibitors caused no major changes in mineral metabolism while of the calcium antagonists studied only verapamil raised the levels of Ca2+ (P < .01). No significant relationship between the changes in mineral metabolism and the reduction in blood pressure was observed in any of the treatment groups. Of the antihypertensive drugs used in the present study, beta-blockers appeared to reverse the basic abnormality with regard to calcium balance, suggesting that the activity of the sympathetic nerve system is involved in the disturbed calcium metabolism seen in hypertensive patients