scholarly journals Mechanisms Involved in the Relationship between Low Calcium Intake and High Blood Pressure

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.

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1748
Author(s):  
Eda Demirel ◽  
Caroline Arnold ◽  
Jaspal Garg ◽  
Marius Andreas Jäger ◽  
Carsten Sticht ◽  
...  

The regulator of G-protein signaling 5 (RGS5) acts as an inhibitor of Gαq/11 and Gαi/o activity in vascular smooth muscle cells (VSMCs), which regulate arterial tone and blood pressure. While RGS5 has been described as a crucial determinant regulating the VSMC responses during various vascular remodeling processes, its regulatory features in resting VSMCs and its impact on their phenotype are still under debate and were subject of this study. While Rgs5 shows a variable expression in mouse arteries, neither global nor SMC-specific genetic ablation of Rgs5 affected the baseline blood pressure yet elevated the phosphorylation level of the MAP kinase ERK1/2. Comparable results were obtained with 3D cultured resting VSMCs. In contrast, overexpression of RGS5 in 2D-cultured proliferating VSMCs promoted their resting state as evidenced by microarray-based expression profiling and attenuated the activity of Akt- and MAP kinase-related signaling cascades. Moreover, RGS5 overexpression attenuated ERK1/2 phosphorylation, VSMC proliferation, and migration, which was mimicked by selectively inhibiting Gαi/o but not Gαq/11 activity. Collectively, the heterogeneous expression of Rgs5 suggests arterial blood vessel type-specific functions in mouse VSMCs. This comprises inhibition of acute agonist-induced Gαq/11/calcium release as well as the support of a resting VSMC phenotype with low ERK1/2 activity by suppressing the activity of Gαi/o.


Nephrology ◽  
2002 ◽  
Vol 7 (1) ◽  
pp. A69-A69 ◽  
Author(s):  
Vlado Perkovic ◽  
Tim D Hewitson ◽  
Kristen J Kelynack ◽  
Marina Martic ◽  
Melanie G Tait ◽  
...  

2010 ◽  
Vol 49 (6) ◽  
pp. 1012-1021 ◽  
Author(s):  
Gyun Jee Song ◽  
Stacey Barrick ◽  
Kristen L. Leslie ◽  
Brian Sicari ◽  
Nathalie M. Fiaschi-Taesch ◽  
...  

1984 ◽  
Vol 247 (6) ◽  
pp. E822-E826 ◽  
Author(s):  
R. C. Stanton ◽  
S. B. Plant ◽  
D. A. McCarron

Parathyroid hormone (PTH) is a vasodilator of vascular smooth muscle tissue. It has been shown to produce this vasodilation in normotensive and hypertensive laboratory rats. The effect is log dose dependent, maximal at 1 min and persists for 3–5 min. The cellular mechanisms involved in PTH-mediated vasodilation are unknown. In this study, we sought to determine the cellular changes of cAMP after administration of bovine (b)PTH (1–34). cAMP content of vascular smooth muscle cells was measured at 30 s, 1, 3, and 5 min after incubation with synthetic bPTH (1–34). Tissue cAMP content was decreased by 55% at 1 min (4.1 +/- 0.5 pmol/mg protein at time 0 vs. 1.9 +/- 0.2 pmol/mg protein at 1 min, P less than 0.001). After 5 min, cAMP levels returned to base-line values and increased over the next 5–10 min to levels above base line (P less than 0.01). In conclusion, our data suggest that the initial response of vascular smooth muscle cells to short-term incubation with bPTH (1–34) is an acute decrease in cAMP content.


2016 ◽  
pp. gfw274 ◽  
Author(s):  
Stacey Dineen Rodenbeck ◽  
Chad A. Zarse ◽  
Mikaela L. McKenney-Drake ◽  
Rebecca S. Bruning ◽  
Michael Sturek ◽  
...  

2015 ◽  
Vol 52 (5) ◽  
pp. 321-333 ◽  
Author(s):  
Mi So Yoon ◽  
Kyung-Jong Won ◽  
Do-Yoon Kim ◽  
Dae Il Hwang ◽  
Seok Won Yoon ◽  
...  

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