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Local renin-angiotensin systems

A H Danser1

  • 1Department of Pharmacology, Cardiovasculair Onderzoeksinstituut Erasmus Universiteit Rotterdam COEUR, The Netherlands.

Molecular and Cellular Biochemistry
|April 12, 1996
PubMed
Summary

The local cardiovascular renin-angiotensin system (RAS) relies on kidney-produced renin. Local angiotensin formation in tissues depends on circulating renin, challenging the idea of an independent local RAS.

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Area of Science:

  • Cardiovascular Physiology
  • Renal Physiology
  • Endocrinology

Background:

  • The local cardiovascular renin-angiotensin system (RAS) is hypothesized to explain RAS inhibitor efficacy in cardiovascular diseases.
  • This hypothesis assumes local angiotensin II formation independent of circulating RAS components.

Purpose of the Study:

  • To investigate the dependence of local angiotensin formation on circulating renin.
  • To reassess the concept of an independent local cardiovascular RAS.

Main Methods:

  • Perfusion of isolated rat hearts and hindlimbs to measure angiotensin release.
  • In vivo measurement of angiotensin production in humans and pigs, accounting for regional angiotensin clearance.
  • Quantification of renin and angiotensin levels in plasma and cardiac tissue before and after nephrectomy in pigs and rats.
  • Analysis of renin binding to cardiac vascular membranes.

Main Results:

  • Angiotensin release from perfused rat organs depended on renal renin.
  • In vivo tissue angiotensin production correlated with plasma renin activity.
  • Cardiac renin and angiotensin levels, and vascular renin and angiotensin in rats, decreased significantly after nephrectomy.
  • Renin was found to bind to cardiac vascular membranes, suggesting uptake from plasma.

Conclusions:

  • Local angiotensin formation in the heart and vessel walls occurs but depends on circulating renal renin.
  • The concept of an independent local cardiovascular RAS requires reassessment.
  • Tissues may regulate local angiotensin levels through mechanisms like renin receptor density and ACE activity.

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