RENAL DIVALENT-CATION EXCRETION IN SECONDARY HYPERTENSION

1. To determine whether abnormal renal calcium excretion is unique to primary genetic hypertension, blood pressure and 24h urinary excretion of calcium, magnesium, sodium and creatinine were measured in deoxycorticosterone-saline and two-kidney, one-clip Goldblatt hypertensive rats and in their respective controls on low (0.2%) and high (1.8%) dietary calcium intakes. 2. Calcium supplementation lowered blood pressure (P<0.05) in deoxycorticosterone-saline rats and in control saline-loaded rats, raised blood pressure in two-kidney, one clip rats, and had no effect in sham-operated control rats. 3. On both diets, calcium excretion was higher in hypertensive than in normotensive rats. The high calcium diet increased urinary calcium excretion in all rats, but the changes in urinary calcium excretion closely paralleled the diet-induced changes in blood pressure. Thus, urinary calcium excretion in deoxycorticosterone-saline animals, in whom calcium lowered blood pressure the most, rose the least (107%). Urinary calcium excretion rose the most in two-kidney, one-clip animals (1113%), whose blood pressure also rose the most. 4. Urinary magnesium excretion was also abnormal in hypertensive rats compared with normotensive rats, falling on the high compared with the low calcium diet in normotensive rats, but not in either hypertensive strain. Furthermore, urinary magnesium excretion was closely linked to urinary calcium excretion in saline-loaded control rats (r=0.78; P=0.008), but was dissociated from urinary calcium excretion in deoxycorticosterone-saline rats (r=0.02; not significant). 5. We conclude (a) that the renal handling of both calcium and magnesium is altered in secondary hypertension, and (b) that dietary calcium supplementation may have different effects on blood pressure in different forms of hypertensive disease. We hypothesize that elevated blood pressure per se may be responsible for the exaggerated calciuresis of hypertension.