Rev Port Cardiol. 1994 Nov;13(11):859-67, 809.

[Molecular pathobiology in heart failure].

Revista portuguesa de cardiologia : orgao oficial da Sociedade Portuguesa de Cardiologia = Portuguese journal of cardiology : an official journal of the Portuguese Society of Cardiology

[Article in Portuguese]
K Reis-Santos, C André, S V Fernandes, F Barros, S Pinto, A M Centeno, P Costa, D Serra, P M Campos, F Godinho

PMID: 7848657

Abstract

Heart failure is a pathophysiological state resulting from disturbed cardiac function. It is based on complex molecular processes, many of which are not fully understood. During heart failure adaptive mechanisms, that reinstall altered cardiac function, are activated. The main mechanisms are: a) Alteration of the structure and composition of myocytes by myocardial hypertrophy, reexpression of fetal and neo-natal proteins and the expression of certain proto-oncogenes; b) Activation of the neuroendocrinal system, specifically the sympathetic nervous system, renin-angiotensin-aldosterone system and vasopressin release; c) Activation of autocrine and paracrine systems. However, when these systems are activated beyond a certain limit they contribute to heart failure aggravation. This can also be promoted by alteration of the calcium metabolism inherent in heart failure. The synthesis of the counterregulator atrial natriuretic factor is also increased.

Substances

• Vasopressins
• Atrial Natriuretic Factor
• Calcium

MeSH terms

• Atrial Natriuretic Factor / metabolism
• Calcium / metabolism
• Cardiomegaly / complications
• Heart Failure* / etiology
• Heart Failure* / metabolism
• Heart Failure* / pathology
• Heart Failure* / physiopathology
• Heart Failure* / therapy
• Humans
• Neurosecretory Systems / physiopathology
• Protein Biosynthesis
• Renin-Angiotensin System / physiology
• Sympathetic Nervous System / physiopathology
• Vasopressins / metabolism

Publication Types

• English Abstract
• Journal Article
• Review