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Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors
12:03

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Angiotensin II-aldosterone interaction in human coronary microarteries involves GPR30, EGFR, and endothelial NO

Wendy W Batenburg1, Pieter M Jansen, Antoon J van den Bogaerdt

  • 1Division of Pharmacology and Vascular Medicine, Department of Internal Medicine, Erasmus MC, Dr Molewaterplein 50, room EE1418b, 3015 GE Rotterdam, The Netherlands.

Cardiovascular Research
|January 21, 2012
PubMed

Insights

Steroids like aldosterone impact blood vessel constriction by angiotensin II. They enhance it at low doses via GPR30 and EGFR, but inhibit it at high doses by activating nitric oxide synthase.

Area of Science:

  • Cardiovascular Biology
  • Endocrinology
  • Pharmacology

Background:

  • The interaction between aldosterone and angiotensin II is crucial in regulating vascular tone.
  • Understanding these interactions in human coronary microarteries (HCMAs) is vital for cardiovascular health.

Purpose of the Study:

  • To investigate the complex interplay between aldosterone and angiotensin II in human coronary microarteries (HCMAs).
  • To elucidate the concentration-dependent effects of steroids on angiotensin II-induced vasoconstriction.

Main Methods:

  • HCMAs from organ donors were subjected to myography.
  • Vascular responses to angiotensin II were measured after pre-incubation with various steroids and specific inhibitors (GPR30, EGFR, NOS, MAPK, ERK).

Main Results:

  • Steroids potentiated angiotensin II-induced constriction at nanomolar concentrations, an effect blocked by GPR30 antagonist G15.
  • At micromolar concentrations, this potentiation was lost or reversed into antagonism, linked to endothelial nitric oxide synthase (eNOS) activation.
  • Epidermal growth factor receptor (EGFR) transactivation was implicated in the potentiation, while eNOS activation mediated the antagonism at higher steroid levels.

Conclusions:

  • Steroids exhibit a biphasic effect on angiotensin II-induced vasoconstriction in HCMAs.
  • Low (nanomolar) steroid concentrations enhance vasoconstriction via GPR30 and EGFR.
  • High (micromolar) steroid concentrations inhibit vasoconstriction through eNOS activation, with specific effects varying by steroid type.
Abstract

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