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Myocardial and plasma renin-angiotensinogen dynamics during pressure-induced cardiac hypertrophy

L J Heller1, J A Opsahl, S E Wernsing

  • 1Department of Medical and Molecular Physiology, University of Minnesota School of Medicine, Duluth 55812, USA.

The American Journal of Physiology
|April 8, 1998
PubMed

Insights

Cardiac hypertrophy in rats shows myocardial renin levels correlate with plasma renin, but this relationship diminishes over time. Renin is found in the interstitial space and generates angiotensin I within the heart.

Area of Science:

  • Cardiovascular Physiology
  • Renal Physiology
  • Cardiac Hypertrophy

Background:

  • Pressure-overload cardiac hypertrophy is a significant cardiovascular condition.
  • The role of local renin-angiotensin system components within the heart requires further elucidation.
  • Understanding myocardial renin and angiotensinogen dynamics is crucial for cardiac disease research.

Purpose of the Study:

  • To investigate the relationship between plasma and left ventricular (LV) renin and angiotensinogen concentrations in a rat model of pressure-overload cardiac hypertrophy.
  • To determine if myocardial renin levels remain proportional to plasma levels over time during the development of cardiac hypertrophy.
  • To assess the functional significance of intramyocardial renin-angiotensinogen system components.

Main Methods:

  • Induction of pressure-overload cardiac hypertrophy via subdiaphragmatic aortic constriction (AC) in rats.
  • Measurement of plasma and LV renin and angiotensinogen concentrations at different time points post-AC.
  • Assessment of renin localization within myocytes and interstitial spaces.
  • In vitro incubation experiments to evaluate angiotensin I generation from myocardial components.

Main Results:

  • LV hypertrophy was evident 3 days after AC and persisted at 42 days.
  • Plasma and LV renin and angiotensinogen levels were not significantly different between AC and sham groups at 42 days.
  • LV renin and angiotensinogen concentrations were approximately 25% and 4% of plasma levels, respectively, throughout the experiment.
  • Myocytes contained little renin, suggesting interstitial localization.
  • Incubation studies demonstrated significant angiotensin I generation by myocardial interstitial renin and angiotensinogen.

Conclusions:

  • In this pressure-overload cardiac hypertrophy model, LV renin levels appear to vary with plasma renin concentrations.
  • Myocardial renin is primarily located in the interstitial space, not within myocytes.
  • The intramyocardial renin-angiotensin system is capable of generating significant amounts of angiotensin I locally within the heart.

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