Salt Appetite and its Effects on Cardiovascular Risk in Primary Aldosteronism

Abstract

First described in 1955 by Jerome W. Conn, primary aldosteronism (PA) today is well established as a relevant cause of secondary hypertension and accounts for about 5–10 % of hypertensives. The importance of considering PA is based on its deleterious target organ damage far beyond the effect of elevated blood pressure and on PA being a potentially curable form of hypertension. Aside the established contributory role of high dietary salt intake to arterial hypertension and cardiovascular disease, high salt intake is mandatory for aldosterone-mediated deleterious effects on target-organ damage in patients with primary aldosteronism. Consequently, counselling patients on the need to reduce salt intake represents a major component in the treatment of PA to minimize cardiovascular damage. Unfortunately, in PA patients salt intake is high and far beyond the target values of 5 g per day, recommended by the World Health Organization. Insufficient patient motivation for lifestyle interventions can be further complicated by enhancing effects of aldosterone on salt appetite, via central and gustatory pathways. In this context, treatment for PA by adrenalectomy results in a spontaneous decrease in dietary salt intake and might therefore provide further reduction of cardiovascular risk in PA than specific medical treatment alone. Furthermore, there is evidence from clinical studies that even after sufficient treatment of PA dietary salt intake remains a relevant prognostic factor for cardiovascular risk. This review will focus on the synergistic benefits derived from both blockade of aldosterone-mediated effects and reduction in dietary salt intake on cardiovascular risk.

Partial Replacement of NaCl with KCl in Cooked Meat Could Reduce the Liver Damage Through Renin–Angiotensin System in Mice

“…[27] Aldosterone, viewed as a hormone controlling sodium reabsorption and potassium excretion in the distal nephron, also plays essential pathogenetic roles in cardiovascular and renal injury. [27,28] This study aims to explore the impact of cooked meat with partial replacement of NaCl with KCl to improve liver damage and to evaluate the protective effects on the liver in terms of lipid metabolism, antioxidant, inflammation, and local RAS in mice, to produce ameliorated sodium-reduced cooked meat in physiological function.…”

“…[ 27 ] Aldosterone, viewed as a hormone controlling sodium reabsorption and potassium excretion in the distal nephron, also plays essential pathogenetic roles in cardiovascular and renal injury. [ 27,28 ]…”

HSD2 neurons are evolutionarily conserved and required for aldosterone-induced salt appetite

“…Despite their excessive sodium retention, patients with aldosteronism occasionally report salt cravings (14)(15)(16), and those with aldosterone-secreting adenomas consume the most sodium (17). Excessive salt intake is particularly problematic in aldosteronism because sodium intake predicts the severity of cardiac complications, including left ventricular hypertrophy (18)(19)(20)(21). Decreasing salt intake reduces blood pressure and may also reduce cardiovascular complications (19)(20)(21)(22)(23), but long-term behavioral recommendations to reduce dietary sodium are notoriously ineffective.…”

Moderate dietary salt restriction improves blood pressure and mental well‐being in patients with primary aldosteronism: The salt CONNtrol trial

“…Aldosterone interferes with sodium homeostasis on multiple levels, including renal and central effects: Animal studies suggested that key neuronal structures involved in the regulation of salt appetite are the nucleus of the solitary tract in an intricate interplay with the central nucleus of the amygdala (CeA) [8][9][10]. In patients with aldosterone excess, such as primary aldosteronism (PA), salt appetite is impaired, which facilitates high dietary salt intake [11,12].…”