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The neurohormonal network in the RAAS can bend before breaking.

Publication ,  Journal Article
Wagman, G; Fudim, M; Kosmas, CE; Panni, RE; Vittorio, TJ
Published in: Curr Heart Fail Rep
June 2012

The renin-angiotensin-aldosterone system (RAAS) has evolved in humans as one of the main physiological networks by which blood pressure and blood flow to vital organs is maintained. The RAAS has evolved to circumvent life-threatening events such as hemorrhage and starvation. Although short-term activation of this system had been well suited to counteract such catastrophes of early man, excessive chronic activation of the RAAS plays a fundamental role in the development and progression of cardiovascular disease in modern man. The RAAS is an intricate network comprising a number of major organ systems (heart, kidney, and vasculature) and signaling pathways. The main protagonists are renin, angiotensinogen (Ang), angiotensin I (Ang I), angiotensin II (Ang II), and aldosterone (Aldo). The study and delineation of each of these substances has allowed modern medicine to create targets by which cardiovascular disease can be treated. The main modulators that have been synthesized in this respect are angiotensin-converting enzyme inhibitors (ACEIs), angiotensin receptor blockers (ARBs), mineralocorticoid receptor blockers (MRBs), and direct renin inhibitors (DRIs). Over the past few decades, each of these substances has proven efficacious to varying degrees amongst a number of clinical settings. Additionally, there exists data for and against the use of these agents in combination. The use of these agents in combination poses a larger question conceptually: can excessive pharmacological inhibition of the RAAS lead to patient harm? This perspective will examine the concept of a neurohormonal inhibition ceiling in pertinent experimental and clinical trials.

Duke Scholars

Published In

Curr Heart Fail Rep

DOI

EISSN

1546-9549

Publication Date

June 2012

Volume

9

Issue

2

Start / End Page

81 / 91

Location

United States

Related Subject Headings

  • Renin-Angiotensin System
  • Neurotransmitter Agents
  • Humans
  • Drug Therapy, Combination
  • Cardiovascular System & Hematology
  • Cardiovascular Diseases
  • Cardiovascular Agents
  • 3201 Cardiovascular medicine and haematology
  • 1103 Clinical Sciences
  • 1102 Cardiorespiratory Medicine and Haematology
 

Citation

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MLA
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Wagman, G., Fudim, M., Kosmas, C. E., Panni, R. E., & Vittorio, T. J. (2012). The neurohormonal network in the RAAS can bend before breaking. Curr Heart Fail Rep, 9(2), 81–91. https://doi.org/10.1007/s11897-012-0091-y
Wagman, Gabriel, Marat Fudim, Constantine E. Kosmas, Robert E. Panni, and Timothy J. Vittorio. “The neurohormonal network in the RAAS can bend before breaking.Curr Heart Fail Rep 9, no. 2 (June 2012): 81–91. https://doi.org/10.1007/s11897-012-0091-y.
Wagman G, Fudim M, Kosmas CE, Panni RE, Vittorio TJ. The neurohormonal network in the RAAS can bend before breaking. Curr Heart Fail Rep. 2012 Jun;9(2):81–91.
Wagman, Gabriel, et al. “The neurohormonal network in the RAAS can bend before breaking.Curr Heart Fail Rep, vol. 9, no. 2, June 2012, pp. 81–91. Pubmed, doi:10.1007/s11897-012-0091-y.
Wagman G, Fudim M, Kosmas CE, Panni RE, Vittorio TJ. The neurohormonal network in the RAAS can bend before breaking. Curr Heart Fail Rep. 2012 Jun;9(2):81–91.
Journal cover image

Published In

Curr Heart Fail Rep

DOI

EISSN

1546-9549

Publication Date

June 2012

Volume

9

Issue

2

Start / End Page

81 / 91

Location

United States

Related Subject Headings

  • Renin-Angiotensin System
  • Neurotransmitter Agents
  • Humans
  • Drug Therapy, Combination
  • Cardiovascular System & Hematology
  • Cardiovascular Diseases
  • Cardiovascular Agents
  • 3201 Cardiovascular medicine and haematology
  • 1103 Clinical Sciences
  • 1102 Cardiorespiratory Medicine and Haematology