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Heart failure: how important is cellular sequestration? The role of the renin-angiotensin-aldosterone system

Walmor C De Mello1

  • 1Department of Pharmacology, Medical Sciences Campus, University Puerto Rico, P.O. Box 365067, San Juan, PR 00936-5067, USA. wmello@rcm.upr.edu

Journal of Molecular and Cellular Cardiology
|July 28, 2004
PubMed

Insights

Heart failure involves complex cellular changes, including impaired cell coupling and fibrosis. This review explores how the renin-angiotensin-aldosterone system contributes to these issues and how ACE inhibitors improve synchronization.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Pathophysiology

Background:

  • Heart failure is characterized by declining heart contractility and involves inflammatory cytokines, endothelin, angiotensin II, and aldosterone.
  • These alterations lead to cellular and molecular changes, impairing cell coupling, impulse propagation, and causing morphologic changes.

Purpose of the Study:

  • To discuss the role of cellular sequestration, impaired cell coupling, and interstitial fibrosis in heart failure development.
  • To describe the involvement of plasma and cardiac renin-angiotensin-aldosterone systems in cellular sequestration.
  • To explore the potential role of an intracellular renin-angiotensin system in intercellular signaling.

Main Methods:

  • Review of existing literature on heart failure pathophysiology.
  • Analysis of the renin-angiotensin-aldosterone system's role in cellular processes.
  • Discussion of the mechanisms of action for angiotensin-converting enzyme inhibitors.

Main Results:

  • Impaired cell coupling and interstitial fibrosis may contribute to cellular sequestration in heart failure.
  • Both plasma and cardiac renin-angiotensin-aldosterone systems are implicated in cellular sequestration.
  • An intracellular renin-angiotensin system might play a role in intercellular signaling.

Conclusions:

  • Angiotensin-converting enzyme inhibitors demonstrate beneficial effects by improving cellular synchronization.
  • Improvements include enhanced cell coupling, cell membrane hyperpolarization, and favorable morphologic remodeling.
  • These effects contribute to decreased interstitial fibrosis and ventricular hypertrophy, ameliorating heart failure progression.

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