scholarly journals Urinary calcium excretion, sodium intake and blood pressure in a multi-ethnic population: results of the Wandsworth Heart and Stroke Study

2001 ◽  
Vol 15 (4) ◽  
pp. 229-237 ◽  
Author(s):  
AM Blackwood ◽  
GA Sagnella ◽  
DG Cook ◽  
FP Cappuccio
Keyword(s):  
Blood Pressure ◽  
Sodium Intake ◽  
Urinary Calcium ◽  
Urinary Calcium Excretion ◽  
Calcium Excretion ◽  
Ethnic Population ◽  
Stroke Study

Change in Blood Pressure during Altered Sodium Intake is not Associated with Calciotropic Hormone Level

1997 ◽  
Vol 93 (2) ◽  
pp. 153-157 ◽  
Author(s):  
Ryoji Ozono ◽  
Tetsuya Oshima ◽  
Hideo Matsuura ◽  
Katsuhiko Ishibashi ◽  
Mitsuaki Watanabe ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Calcium Metabolism ◽  
Sodium Intake ◽  
Urinary Calcium ◽  
Urinary Calcium Excretion ◽  
Mean Blood Pressure ◽  
Calcium Excretion ◽  
Sodium Restriction ◽  
Sodium Diet ◽  
Change In Mean

1. We evaluated the effects of the dietary restriction of sodium chloride on blood pressure and systemic calcium metabolism in 19 in-patients with essential hypertension (11 men and 8 women, mean age 49.9 ± 12.1 years). 2. All patients received a high-sodium diet (250 mmol/day) for 1 week, followed by a low-sodium diet (10 mmol/day) for another week. Intake of potassium (100 mmol/day) and of calcium (15 mmol/day) were kept constant throughout the study. 3. Sodium restriction significantly reduced the mean blood pressure (from 114.0 ± 1.9 to 105.0 ± 13.7 mmHg, P < 0.01). Urinary calcium excretion was significantly reduced (from 5.1 ± 2.4 to 2.2 ± 1.0 mmol/day, P < 0.01). 4. The change in mean blood pressure after sodium restriction was not correlated with a change in any parameter of calcium metabolism [whole blood ionized calcium, plasma intact parathyroid hormone, or 1,25-(OH)2 vitamin D3]. 5. Plasma renin activity during a regular sodium diet, an index of renin status, was significantly and inversely correlated with the change in blood pressure during sodium restriction, but not with any change in the parameters of calcium metabolism. 6. We conclude that sodium restriction reduces blood pressure and decreases urinary calcium excretion. However, we observed no significant role of extracellular calcium concentration or of calciotropic hormone concentration in the mechanism of sodium sensitivity.

Urinary Calcium Excretion at Extremes of Sodium Intake in Normal Man

1981 ◽  
Vol 1 (2) ◽  
pp. 84-90 ◽  
Author(s):  
David A. McCarron ◽  
Laura I. Rankin ◽  
William M. Bennett ◽  
Siegfried Krutzik ◽  
Michael R. McClung ◽  
...  
Keyword(s):  
Sodium Intake ◽  
Urinary Calcium ◽  
Urinary Calcium Excretion ◽  
Calcium Excretion ◽  
Normal Man

Renal divalent cation excretion in secondary hypertension

1992 ◽  
Vol 83 (5) ◽  
pp. 561-565 ◽  
Author(s):  
Mario Barbagallo ◽  
Lawrence M. Resnick ◽  
R. Ernest Sosa ◽  
Mary Lou Corbett ◽  
John H. Laragh
Keyword(s):  
Blood Pressure ◽  
Calcium Supplementation ◽  
Dietary Calcium ◽  
Secondary Hypertension ◽  
Urinary Calcium ◽  
Urinary Calcium Excretion ◽  
Calcium Excretion ◽  
Hypertensive Rats ◽  
Calcium Diet ◽  
Magnesium Excretion

1. To determine whether abnormal renal calcium excretion is unique to primary genetic hypertension, blood pressure and 24 h 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.

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