The neuroendocrine-immune interface gone awry in aldosteronism

Extract

See article by Lal et al. (pages 437-447) in this issue.

Congestive heart failure (CHF), a clinical syndrome with characteristic signs and symptoms, is a salt-avid state whose origins are rooted in neurohormonal activation, including the circulating renin-angiotensin-aldosterone system (RAAS). A systemic illness accompanies CHF and contributes to a progressive downhill clinical course and poor prognosis. Features include: (a) oxi/nitrosative stress in such diverse tissues as skin, skeletal muscle, heart, lymphocytes and monocytes; (b) a proinflammatory phenotype involving multiple tissues and blood and expressed as elevated levels of chemokines and such cytokines as IL-6 and TNF-α; and (c) a catabolic state with loss of lean tissue, fat and bone that eventuates in a wasting syndrome termed cardiac cachexia. The pathophysiology of CHF includes a neuroendocrine-immune interface gone awry. This brief commentary, prepared in response to the study from the Leenen laboratory in Ottawa [1], focuses on this interface in aldosteronism. Apologies are extended for the limited discussion and literature citations dictated by space constraints.