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Published on: June 14, 2016

Experimental cardiac fibrosis: differential time course of responses to mineralocorticoid-salt administration

G Fujisawa1, R Dilley, M J Fullerton

  • 1Baker Medical Research Institute, Melbourne, Victoria 8008, Australia.

Endocrinology
|July 19, 2001
PubMed

Insights

Mineralocorticoid excess rapidly triggers cardiac fibrosis. Early changes include inflammation and apoptosis by day 4, leading to collagen deposition and elevated blood pressure within weeks in rats.

Area of Science:

  • Cardiovascular Science
  • Endocrinology
  • Pathology

Background:

  • Mineralocorticoids rapidly affect epithelial tissues, but cardiovascular responses appear delayed.
  • Understanding the early cardiac response to mineralocorticoids is crucial for cardiovascular disease research.

Purpose of the Study:

  • To investigate the time course and pattern of early cardiac fibrosis development in a mineralocorticoid-salt rat model.
  • To elucidate the sequence of events following acute mineralocorticoid elevation.

Main Methods:

  • Uninephrectomized rats received deoxycorticosterone injections and mineralocorticoid-rich drinking solution.
  • Rats were humanely killed at various time points (2, 4, 8, 16, 32 days) for analysis.
  • Evaluated changes included type III collagen deposition, blood pressure, inflammatory cell infiltration, and apoptosis.

Main Results:

  • Type III collagen increased from day 2, and blood pressure elevated from day 4.
  • Marked perivascular inflammatory cell infiltration was observed at days 4 and 8.
  • Apoptosis occurred in perivascular areas (days 4-8) and scar areas (days 8-32).

Conclusions:

  • Inappropriate elevation of mineralocorticoid hormones initiates a cascade of cardiac changes.
  • These changes involve cardiac vessels and myocytes, culminating in fibrosis and collagen deposition.
  • Acute mineralocorticoid elevation via bolus injection reveals early cardiac changes within 2 days, contrasting with slower responses in infusion studies.

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