Figure 1.

In low-renin hypertension associated with chronic aldosteronism, heightened urinary and fecal losses of Ca²⁺ lead to ionized hypocalcemia that, in turn, stimulates increased secretion of parathyroid hormone (PTH) by the parathyroid glands. The appearance of secondary hyperparathyroidism (SHPT) provokes increased resorption of bone minerals and augmented absorption and reabsorption of these cations from the gut and kidney, respectively. Characterized as a Ca²⁺ paradox, PTH-mediated intracellular Ca²⁺ overloading leads to the induction of oxidative and nitrosative stress that eventuates in cardiomyocyte necrosis and subsequent replacement fibrosis, or scarring.