Related Experiment Video

Updated: Jun 28, 2026

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

Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors

Published on: June 7, 2016

Angiotensin II type 2 receptor blockade increases bone mass

Yayoi Izu1, Fumitaka Mizoguchi, Aya Kawamata

  • 1Department of Molecular Pharmacology, Medical Research Institute, Tokyo Medical and Dental University, Tokyo 101-0062, Japan.

The Journal of Biological Chemistry
|November 14, 2008
PubMed

Insights

The renin-angiotensin system (RAS) is present in adult bone. Blocking the angiotensin II type 2 (AT2) receptor increases bone mass by boosting bone-forming cells and reducing bone-resorbing cells.

Area of Science:

  • Endocrinology
  • Bone Biology
  • Physiology

Background:

  • The renin-angiotensin system (RAS) is a key regulator of blood pressure and fluid balance.
  • Emerging evidence suggests local roles for RAS components, including in bone cell regulation.
  • The in vivo presence and function of RAS in adult bone remain largely uncharacterized.

Purpose of the Study:

  • To investigate the presence of RAS components in adult bone tissue in vivo.
  • To determine the effect of angiotensin II type 2 (AT2) receptor blockade on bone mass.

Main Methods:

  • Immunohistochemistry was used to detect AT2 receptor, renin, and angiotensin II-converting enzyme in adult bone cells.
  • Administration of an AT2 receptor blocker was employed to assess its impact on bone mass.

Main Results:

  • AT2 receptor protein was found in both osteoblasts and osteoclasts.
  • Renin and angiotensin II-converting enzyme were expressed in bone cells in vivo.
  • Treatment with an AT2 receptor blocker significantly increased bone mass by enhancing osteoblastic activity and suppressing osteoclastic activity.

Conclusions:

  • RAS components are present and active in adult bone tissue.
  • Blockade of the AT2 receptor represents a potential therapeutic strategy for modulating bone mass.

More Related Videos

Subcutaneous Angiotensin II Infusion using Osmotic Pumps Induces Aortic Aneurysms in Mice07:21

Subcutaneous Angiotensin II Infusion using Osmotic Pumps Induces Aortic Aneurysms in Mice

Published on: September 28, 2015

Related Concept Videos

Antihypertensive Drugs: Angiotensin II Receptor Blockers01:30

Antihypertensive Drugs: Angiotensin II Receptor Blockers

In the renin-angiotensin-aldosterone system, a hormone called angiotensin II plays a crucial role. It binds to the AT1 receptors in vascular smooth muscles coupled with Gq proteins. The activation of these receptors activates an enzyme called phospholipase C, which releases two molecules: inositol trisphosphate and diacylglycerol. These molecules cause a chain reaction that leads to the phosphorylation of myosin light chains and promotes interaction between actin and myosin, leading to smooth...
Antihypertensive Drugs: Direct Renin Inhibitors01:25

Antihypertensive Drugs: Direct Renin Inhibitors

The renin-angiotensin-aldosterone system (RAAS) is an intricate physiological pathway involving numerous enzymes and hormones, including renin, angiotensin-converting enzyme (ACE), angiotensin I and II, and aldosterone. Imbalances within this system increase the production of angiotensin II and aldosterone. Increased angiotensin II levels promote vasoconstriction and blood pressure elevation. Concurrently, higher aldosterone levels stimulate sodium and water reabsorption in the kidneys,...
Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors01:30

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors

Angiotensin-converting enzyme (ACE), a vital component of the renin-angiotensin-aldosterone system, is abundant in lung endothelial cells. ACE converts the inactive decapeptide, angiotensin I, into the active octapeptide, angiotensin II. This potent vasoconstrictor narrows blood vessels, increasing resistance to blood flow and elevating blood pressure. Angiotensin II also stimulates aldosterone production, encouraging kidney cells to reabsorb more sodium and water from urine, thereby increasing...
Antihypertensive Drugs: Action of β1 Blockers01:17

Antihypertensive Drugs: Action of β1 Blockers

β1-receptors are primarily located in the heart and kidneys. In cardiac myocytes, these receptors interact with neurotransmitters released by the sympathetic nervous system during heightened activity or danger. As a result, β1-receptors get activated, initiating a series of biochemical processes. Excessive activation of beta receptors due to chronic stress can abnormally increase heart rate and contractility, resulting in high blood pressure or hypertension. To counteract this, β1-blockers...
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
Antihypertensive Drugs: Action of Calcium Channel Blockers01:18

Antihypertensive Drugs: Action of Calcium Channel Blockers

Calcium ions are essential to contract smooth muscle cells in blood vessels. They enter these cells through voltage-dependent calcium channels, specifically L-type calcium channels in the cell membrane. These L-type calcium channels are integral to the excitation-contraction coupling process in smooth muscle. When a stimulus is received by smooth muscle cells, their membrane depolarizes. This alteration in membrane potential instigates the opening of L-type calcium channels. As a result,...