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The neuroendocrine-immune interface gone awry in aldosteronism.
| Content Provider | Semantic Scholar |
|---|---|
| Author | Weber, Karl T. |
| Copyright Year | 2004 |
| Abstract | 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. The body's trillions of cells are organized into specialized tissues (e.g., epi- and endothelium, lymphoid cells of respiratory and gastrointestinal mucosae) and organs. Together, they serve as functional units integral to preserving homeostasis, such as the regulation of respiratory gas exchange, the composition and osmotic balance of the internal environment, or extracellular fluid, and the immune system. The neuroendocrine and immune systems are linked together because they share ligands and receptors. This common “chemical language” promotes their bidirectional communication and integrative physiology [2]. Neurotransmitters, neuropeptides and … *Tel.: +1 901 448 5750; fax: +1 901 448 8084. Email address: KTWeber{at}utmem.edu |
| File Format | PDF HTM / HTML |
| DOI | 10.1016/j.cardiores.2004.08.015 |
| PubMed reference number | 15537489 |
| Journal | Medline |
| Volume Number | 64 |
| Issue Number | 3 |
| Alternate Webpage(s) | https://oup.silverchair-cdn.com/oup/backfile/Content_public/Journal/cardiovascres/64/3/10.1016/j.cardiores.2004.08.015/2/64-3-381.pdf?Expires=1492034464&Key-Pair-Id=APKAIUCZBIA4LVPAVW3Q&Signature=Rg~Q6HPTpIwJlCh-uk3pXwoAFM23to3m3OdtjIbUu7FO-qW1yekZwWsRpSpNa3LbSFh4UY3PtgWQEOWH85NmNf0x2dsyk0Rwt4F55xKzDWMC4X~874IyNB3mkPPrnDVzPpuhbhNxkpQHLT3kTlWdqBBcS1RA4-kj8qzBokAitQoYQg9kcF6JLEYz~kAmi-zBPqVGMGM43ex2hz6D~TOgLVfMWM83~X0X1RKsjNUVPLhhkDOdYxwK4F7EY740Pif0TZZWAH9hHWRv2vb7UQQNckzCYSYHNCNrDgWmmZ6t3j2M~v~bXMLf1TLmAaJi42uGoNMjUIdtT26jvL8TP7nXhA__ |
| Alternate Webpage(s) | http://cardiovascres.oxfordjournals.org/content/64/3/381.full.pdf |
| Alternate Webpage(s) | https://doi.org/10.1016/j.cardiores.2004.08.015 |
| Journal | Cardiovascular research |
| Language | English |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |
