Salt, Aldosterone, and Parathyroid Hormone: What Is the Relevance for Organ Damage?

Abstract

Structured interventions on lifestyle have been suggested as a cost-effective strategy for prevention of cardiovascular disease. Epidemiologic studies demonstrate that dietary salt restriction effectively decreases blood pressure, but its influence on cardiovascular morbidity and mortality is still under debate. Evidence gathered from studies conducted in patients with primary aldosteronism, essential hypertension, or heart failure demonstrates that long-term exposure to elevated aldosterone results in cardiac structural and functional changes that are independent of blood pressure. Animal experiments and initial clinical studies indicate that aldosterone damages the heart only in the context of an inappropriately elevated salt status. Recent evidence suggests that aldosterone might functionally interact with the parathyroid hormone and thereby affect calcium homeostasis with important sequelae for bone mineral density and strength. The interaction between aldosterone and parathyroid hormone might have implications also for the heart. Elevated dietary salt is associated on the one hand with increased urinary calcium excretion and, on the other hand, could facilitate the interaction between aldosterone and parathyroid hormone at the cellular level. This review summarizes the evidence supporting the contribution of salt and aldosterone to cardiovascular disease and the possible cardiac and skeletal consequences of the mutual interplay between aldosterone, parathyroid hormone, and salt.

Positive association between metabolic syndrome and bone mineral density among Malaysians

“…This observation contradicts the findings of a meta-analysis, which showed that blood pressure is negatively associated with BMD and positively with increased risk of osteoporosis [40]. It is generally agreed that high blood pressure increases the excretion of calcium, thus elevating parathyroid hormone level and bone resorption [9]. We suggest that increased systolic blood pressure is reflective of increased body size, which increases the peripheral resistance of the vascular system [41], thus explaining the positive association with BMD.…”

“…Diabetes and obesity are associated with bone marrow adipogenesis which deprives mesenchymal stem cells available for osteoblast formation 7 . Hypertension increases excretion of calcium, elevating parathyroid secretion and bone resorption 9 . Oxidized low-density lipoprotein cholesterol particles and excess free fatty acids in dyslipidaemia can uncouple bone remodelling 10 - 13 , favouring bone resorption.…”

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

“…A bidirectional stimulating relationship between PTH and aldosterone is reported. Patients with primary aldosteronism have high levels of PTH that return to physiological concentration after the adenoma removal or pharmacological treatment with aldosterone antagonists [106]. Similarly, hypertension associated with secondary aldosteronism due to hyperparathyroidism resolves after parathyroidectomy [107,108].…”

Resistant Hypertension: A Clinical Case

“…H ypertension causes significant morbidity and mortality worldwide, having a prevalence of about 30 % of the adult world population, and around 85 % of them above 55 years-old (1,2). Hypertension has the largest prevalence of all cardiovascular risk factors and, due to its deleterious effects on the cardiovascular and renal systems, it is considered responsible for 45 % of the heart disease related deaths and 51 % of them due to stroke (1, 3).…”