Relationship of blood pressure, calcium intake, and parathyroid hormone

1989 ◽  
Vol 49 (1) ◽  
pp. 183-184 ◽  
Author(s):  
J Villar ◽  
J Repke ◽  
J Belizan
Hypertension ◽  
2000 ◽  
Vol 35 (5) ◽  
pp. 1154-1159 ◽  
Author(s):  
Rolf Jorde ◽  
Johan Sundsfjord ◽  
Egil Haug ◽  
Kaare H. Bønaa

Nutrients ◽  
2019 ◽  
Vol 11 (5) ◽  
pp. 1112 ◽  
Author(s):  
Cecilia Villa-Etchegoyen ◽  
Mercedes Lombarte ◽  
Natalia Matamoros ◽  
José M. Belizán ◽  
Gabriela Cormick

There is increasing epidemiologic and animal evidence that a low calcium diet increases blood pressure. The aim of this review is to compile the information on the link between low calcium intake and blood pressure. Calcium intake may regulate blood pressure by modifying intracellular calcium in vascular smooth muscle cells and by varying vascular volume through the renin–angiotensin–aldosterone system. Low calcium intake produces a rise of parathyroid gland activity. The parathyroid hormone increases intracellular calcium in vascular smooth muscles resulting in vasoconstriction. Parathyroidectomized animals did not show an increase in blood pressure when fed a low calcium diet as did sham-operated animals. Low calcium intake also increases the synthesis of calcitriol in a direct manner or mediated by parathyroid hormone (PTH). Calcitriol increases intracellular calcium in vascular smooth muscle cells. Both low calcium intake and PTH may stimulate renin release and consequently angiotensin II and aldosterone synthesis. We are willing with this review to promote discussions and contributions to achieve a better understanding of these mechanisms, and if required, the design of future studies.


2003 ◽  
Vol 285 (5) ◽  
pp. H1882-H1889 ◽  
Author(s):  
Pasi Jolma ◽  
Peeter Kööbi ◽  
Jarkko Kalliovalkama ◽  
Mika Kähönen ◽  
Meng Fan ◽  
...  

Chronic renal failure (CRF) is associated with abnormal lipid metabolism and high prevalence of vascular complications. Calcium salts are commonly used in CRF as phosphate binders. Increased calcium intake may also lower plasma cholesterol and beneficially influence vascular tone. Therefore, we investigated the influence of increasing dietary calcium from 0.3% to 3.0% for 8 wk after 5/6 nephrectomy (NTX) on plasma cholesterol and mesenteric resistance vessel tone in male Sprague-Dawley rats. The groups were Sham, Sham-Calcium, NTX, and NTX-Calcium ( n = 10–11). Blood pressure was modestly elevated after NTX, whereas the plasma creatinine, urea nitrogen, phosphate, and parathyroid hormone levels were clearly increased. The high-calcium diet suppressed plasma phosphate and parathyroid hormone but was without effect on blood pressure. The NTX resulted in 1.6-fold elevation in plasma total cholesterol and 40% reduction in high density-to-low density lipoprotein ratio (HDL/LDL). However, the lipid profile in NTX rats on the high-calcium diet did not differ from sham-operated controls. The endothelium-mediated relaxations induced by acetylcholine were impaired in NTX rats, whereas the response was normalized by a high-calcium diet. No differences in vasorelaxations by the endothelium-independent vasodilator nitroprusside were detected. In conclusion, improved vasorelaxation after a high-calcium diet could be due to reduced plasma total cholesterol and ameliorated HDL/LDL ratio, although decreased plasma phosphate and parathyroid hormone may also play a significant role in the vascular effects of increased calcium intake.


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