Dietary calcium intake is inversely associated with blood pressure in Brazilian children

2016 ◽  
Vol 68 (3) ◽  
pp. 331-338 ◽  
Author(s):  
Elma Izze da Silva Magalhães ◽  
Milene Cristine Pessoa ◽  
Sylvia do Carmo Castro Franceschini ◽  
Juliana Farias Novaes
1995 ◽  
Vol 142 (9) ◽  
pp. 935-945 ◽  
Author(s):  
F. P. Cappuccio ◽  
P. Elliott ◽  
P. S. Allender ◽  
J. Pryer ◽  
D. A. Follman ◽  
...  

1992 ◽  
Vol 21 (4) ◽  
pp. 683-689 ◽  
Author(s):  
EMERENTIA C H VAN BERESTEIJN ◽  
MARIJKE RIEDSTRA ◽  
ANNEMARIE VAN DER WEL ◽  
EVERT G SCHOUTEN ◽  
JAN BUREMA ◽  
...  

Maturitas ◽  
1993 ◽  
Vol 16 (3) ◽  
pp. 204-205
Author(s):  
E.C.H. Van Beresteijn ◽  
M. Riedstra ◽  
A. Van der Wel ◽  
E.G. Schouten ◽  
J. Burema ◽  
...  

1994 ◽  
Vol 72 (8) ◽  
pp. 937-944 ◽  
Author(s):  
David A. McCarron ◽  
Daniel Hatton ◽  
Jean-Baptiste Roullet ◽  
Chantal Roullet

The association between dietary calcium intake, calcium metabolism, and blood pressure form the basis of this review. Epidemiologic data consistently show an inverse relationship between dietary calcium and blood pressure. Clinical trials of calcium supplementation have not been as consistent in outcome. Approximately two-thirds of the supplementation studies have found a beneficial effect of calcium on blood pressure. The lack of consistency in outcome from the clinical trials relative to the epidemiological literature may be related to calcium intake. The epidemiological literature indicates an inverse relationship between calcium intake and blood pressure, with those individuals with the lowest calcium intake (< 700 mg/day) having the highest blood pressure. Clinical studies utilizing patients with high baseline calcium levels (> 700 mg/day) may not see an effect of calcium supplementation on blood pressure because of a ceiling effect. Supplemental calcium appears to correct a defect in calcium handling characterized by a renal calcium leak, increased circulating parathroid hormone, and increased intracellular calcium levels. In part, the deficit in cellular calcium homeostasis may be a consequence of abnormal calmodulin activity. Specifically, it appears that calmodulin activity is diminished in experimental hypertension and that increasing dietary calcium may improve calmodulin activity in the spontaneously hypertensive rat. The deficit in calmodulin activity has the potential to interfere with a number of cellular processes crucial to the regulation of cell function and maintenance of appropriate vascular tone. It is concluded that additional research should be directed toward understanding the ramifications of altered calmodulin activity in hypertension and the influence that dietary calcium can have on the activity of calmodulin.Key words: hypertension, dietary Ca2+, calmodulin, Ca2+ metabolism, calcium channel blockers.


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