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Antihypertensive Drugs: Angiotensin II Receptor Blockers

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Related Experiment Video

Updated: Jul 11, 2026

Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors

Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors

Published on: June 7, 2016

[Angiotensin type 2 receptor-dependent vasodilation].

Katsutoshi Yayama¹, Hiroshi Okamoto

¹Laboratory of Cardiovascular Pharmacology, Department of Biopharmaceutical Sciences, Kobe Gakuin University, Minatojima, Kobe, Japan.

Yakugaku Zasshi : Journal of the Pharmaceutical Society of Japan

|September 11, 2007

Summary

Hypertension up-regulates angiotensin II type 2 (AT2) receptors via AT1 receptors, activating a protective vasodilatory pathway. This AT2 receptor activation contributes to the blood pressure-lowering effects of AT1 receptor blockers.

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Last Updated: Jul 11, 2026

Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors

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Area of Science:

Cardiovascular Physiology
Renal Physiology
Molecular Pharmacology

Context:

Angiotensin II (Ang II) signaling involves AT(1) and AT(2) receptors.
AT(1) receptor activation drives Ang II-dependent hypertension.
AT(2) receptor's protective role in blood pressure regulation is proposed but mechanistically unclear.

Purpose:

To elucidate the mechanisms by which increased AT(2) receptors counterbalance AT(1)-mediated actions of Ang II.
To investigate the role of AT(2) receptor upregulation in hypertensive models.

Summary:

Abdominal aortic banding and Goldblatt hypertension models induce AT(2) receptor upregulation in the thoracic aorta.
AT(1) receptor antagonists, but not calcium antagonists, abolish AT(2) receptor upregulation and hypertension.
Ang II binding to upregulated AT(2) receptors triggers vasodilation via bradykinin B(2) receptor-mediated eNOS phosphorylation and nitric oxide production.

Impact:

Demonstrates that AT(2) receptor upregulation in hypertension is Ang II/AT(1) receptor-dependent.
Reveals a novel AT(2) receptor-mediated vasodilatory pathway involving bradykinin, nitric oxide, and cGMP.
Suggests that AT(2) receptor activation is a key component of the antihypertensive effects of AT(1)-receptor blockers.