Figure 2.

Scheme of the mechanisms involved in the rise of blood pressure in low calcium intake via an increase in cardiac output. Low calcium intake decreased the plasmatic calcium concentration ([Ca²⁺]_plasma), stimulating PTH and the renin–angiotensin–aldosterone system (RAAS). Both angiotensin II and PTH were increased aldosterone secretion due to the adrenal gland. Aldosterone upregulates epithelial sodium channels (ENaC) in the principal cells of the collecting duct in the kidney, increasing apical membrane permeability for Na⁺, thus Na⁺ and water reabsorption. The rise of extracellular fluid volume (ECF) increased cardiac output and hence blood pressure.