A Neuroendocrine-Immune Interface

The Immunostimulatory State of Aldosteronism

Research output: Contribution to journalReview article

8 Citations (Scopus)

Abstract

Hypertension is an important determinant of heart failure. Ventricular systolic and/or diastolic dysfunction can eventuate in an activation of the renin-angiotensin-aldosterone system (RAAS). Circulating RAAS effector hormones lead to: the appearance of the congestive heart failure syndrome; and a systemic illness that features oxi/nitrosative stress in various tissues, including blood, together with circulating pro-inflammatory cytokines, anorexia and, ultimately, cachexia. In addition to its well-known endocrine properties, expressed in epithelial cells of classic target tissues, aldosterone (ALDO) has an emerging portfolio of actions in nonclassic target tissues, such as circulating lymphocytes and monocytes (or peripheral blood mononuclear cells [PBMC]). This neuroendocrine-immune interface is based on Na +-dependent, ALDO-induced iterations in PBMC cytosolic free [Mg 2+]i and [Ca2+]i. Ca2+ loading contributes to an induction of oxi/nitrosative stress and activation of PBMC transcriptome. This immunostimulatory state begets a pro-inflammatory/fibrogenic vascular phenotype involving the heart and systemic organs and can be prevented by either ALDO receptor antagonism or antioxidant. The established efficacy of ALDO receptor antagonism as an integral component of the overall management of symptomatic heart failure may include its immunomodulatory properties. This brief review traces studies that led to and then identified the neuroendocrine-immune interface that accompanies aldosteronism.

Original languageEnglish (US)
Pages (from-to)692-701
Number of pages10
JournalHerz
Volume28
Issue number8
DOIs
StatePublished - Dec 1 2003

Fingerprint

Hyperaldosteronism
Mineralocorticoid Receptors
Blood Cells
Heart Failure
Renin-Angiotensin System
Aldosterone
Cachexia
Anorexia
Transcriptome
Blood Vessels
Monocytes
Antioxidants
Epithelial Cells
Hormones
Lymphocytes
Cytokines
Hypertension
Phenotype
Formoterol Fumarate

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine

Cite this

A Neuroendocrine-Immune Interface : The Immunostimulatory State of Aldosteronism. / Weber, Karl.

In: Herz, Vol. 28, No. 8, 01.12.2003, p. 692-701.

Research output: Contribution to journalReview article

@article{1fd72763f5bb4a7e959083efd29d9b26,
title = "A Neuroendocrine-Immune Interface: The Immunostimulatory State of Aldosteronism",
abstract = "Hypertension is an important determinant of heart failure. Ventricular systolic and/or diastolic dysfunction can eventuate in an activation of the renin-angiotensin-aldosterone system (RAAS). Circulating RAAS effector hormones lead to: the appearance of the congestive heart failure syndrome; and a systemic illness that features oxi/nitrosative stress in various tissues, including blood, together with circulating pro-inflammatory cytokines, anorexia and, ultimately, cachexia. In addition to its well-known endocrine properties, expressed in epithelial cells of classic target tissues, aldosterone (ALDO) has an emerging portfolio of actions in nonclassic target tissues, such as circulating lymphocytes and monocytes (or peripheral blood mononuclear cells [PBMC]). This neuroendocrine-immune interface is based on Na +-dependent, ALDO-induced iterations in PBMC cytosolic free [Mg 2+]i and [Ca2+]i. Ca2+ loading contributes to an induction of oxi/nitrosative stress and activation of PBMC transcriptome. This immunostimulatory state begets a pro-inflammatory/fibrogenic vascular phenotype involving the heart and systemic organs and can be prevented by either ALDO receptor antagonism or antioxidant. The established efficacy of ALDO receptor antagonism as an integral component of the overall management of symptomatic heart failure may include its immunomodulatory properties. This brief review traces studies that led to and then identified the neuroendocrine-immune interface that accompanies aldosteronism.",
author = "Karl Weber",
year = "2003",
month = "12",
day = "1",
doi = "10.1007/s00059-003-2511-y",
language = "English (US)",
volume = "28",
pages = "692--701",
journal = "Herz",
issn = "0340-9937",
publisher = "Urban und Vogel",
number = "8",

}

TY - JOUR

T1 - A Neuroendocrine-Immune Interface

T2 - The Immunostimulatory State of Aldosteronism

AU - Weber, Karl

PY - 2003/12/1

Y1 - 2003/12/1

N2 - Hypertension is an important determinant of heart failure. Ventricular systolic and/or diastolic dysfunction can eventuate in an activation of the renin-angiotensin-aldosterone system (RAAS). Circulating RAAS effector hormones lead to: the appearance of the congestive heart failure syndrome; and a systemic illness that features oxi/nitrosative stress in various tissues, including blood, together with circulating pro-inflammatory cytokines, anorexia and, ultimately, cachexia. In addition to its well-known endocrine properties, expressed in epithelial cells of classic target tissues, aldosterone (ALDO) has an emerging portfolio of actions in nonclassic target tissues, such as circulating lymphocytes and monocytes (or peripheral blood mononuclear cells [PBMC]). This neuroendocrine-immune interface is based on Na +-dependent, ALDO-induced iterations in PBMC cytosolic free [Mg 2+]i and [Ca2+]i. Ca2+ loading contributes to an induction of oxi/nitrosative stress and activation of PBMC transcriptome. This immunostimulatory state begets a pro-inflammatory/fibrogenic vascular phenotype involving the heart and systemic organs and can be prevented by either ALDO receptor antagonism or antioxidant. The established efficacy of ALDO receptor antagonism as an integral component of the overall management of symptomatic heart failure may include its immunomodulatory properties. This brief review traces studies that led to and then identified the neuroendocrine-immune interface that accompanies aldosteronism.

AB - Hypertension is an important determinant of heart failure. Ventricular systolic and/or diastolic dysfunction can eventuate in an activation of the renin-angiotensin-aldosterone system (RAAS). Circulating RAAS effector hormones lead to: the appearance of the congestive heart failure syndrome; and a systemic illness that features oxi/nitrosative stress in various tissues, including blood, together with circulating pro-inflammatory cytokines, anorexia and, ultimately, cachexia. In addition to its well-known endocrine properties, expressed in epithelial cells of classic target tissues, aldosterone (ALDO) has an emerging portfolio of actions in nonclassic target tissues, such as circulating lymphocytes and monocytes (or peripheral blood mononuclear cells [PBMC]). This neuroendocrine-immune interface is based on Na +-dependent, ALDO-induced iterations in PBMC cytosolic free [Mg 2+]i and [Ca2+]i. Ca2+ loading contributes to an induction of oxi/nitrosative stress and activation of PBMC transcriptome. This immunostimulatory state begets a pro-inflammatory/fibrogenic vascular phenotype involving the heart and systemic organs and can be prevented by either ALDO receptor antagonism or antioxidant. The established efficacy of ALDO receptor antagonism as an integral component of the overall management of symptomatic heart failure may include its immunomodulatory properties. This brief review traces studies that led to and then identified the neuroendocrine-immune interface that accompanies aldosteronism.

UR - http://www.scopus.com/inward/record.url?scp=0346096502&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0346096502&partnerID=8YFLogxK

U2 - 10.1007/s00059-003-2511-y

DO - 10.1007/s00059-003-2511-y

M3 - Review article

VL - 28

SP - 692

EP - 701

JO - Herz

JF - Herz

SN - 0340-9937

IS - 8

ER -