Related Experiment Video

Updated: Jul 8, 2026

Subcutaneous Angiotensin II Infusion using Osmotic Pumps Induces Aortic Aneurysms in Mice
07:21

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

Published on: September 28, 2015

Angiotensin increases aldosterone synthase mRNA levels in human NCI-H295 cells

O B Holland1, J M Mathis, I M Bird

  • 1Department of Internal Medicine, University of Texas Medical Branch at Galveston 77555-1060.

Molecular and Cellular Endocrinology
|August 1, 1993
PubMed

Insights

Human adrenocortical NCI-H295 cells respond to angiotensin II stimulation, increasing aldosterone production and aldosterone synthase mRNA. This cell model is valuable for studying aldosterone secretion regulation.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Cell Biology

Background:

  • Aldosterone secretion regulation is crucial for blood pressure control.
  • A lack of chronically responsive cell culture models has hindered research.
  • Human adrenocortical tumor cells (NCI-H295) express key steroidogenic pathways.

Purpose of the Study:

  • To evaluate NCI-H295 cells as a model for studying aldosterone regulation.
  • To determine the effect of angiotensin II and forskolin on aldosterone production and aldosterone synthase (AS) mRNA levels.

Main Methods:

  • NCI-H295 cells were cultured and treated with varying concentrations of angiotensin II (AII) and forskolin.
  • Aldosterone production was measured.
  • Aldosterone synthase (AS, P45011B2) mRNA levels were quantified.

Main Results:

  • Both AII and forskolin stimulated aldosterone production and increased AS mRNA levels in NCI-H295 cells.
  • Angiotensin II demonstrated a greater effect than forskolin.
  • A dose-dependent increase in AS mRNA levels was observed with increasing AII concentrations, paralleling aldosterone production.

Conclusions:

  • NCI-H295 cells provide a valuable human cell culture model for investigating the mechanisms of aldosterone secretion.
  • This model system is responsive to chronic angiotensin II stimulation, addressing a previous research limitation.

More Related Videos

Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors12:03

Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors

Published on: June 7, 2016

Improved Renal Denervation Mitigated Hypertension Induced by Angiotensin II Infusion08:35

Improved Renal Denervation Mitigated Hypertension Induced by Angiotensin II Infusion

Published on: May 26, 2022

Related Concept Videos

Hormonal Regulation01:33

Hormonal Regulation

The renin-aldosterone system is an endocrine system which guides the renal absorption of water and electrolytes, thus managing blood pressure and osmoregulation. Activation of the system begins in the kidneys with a small cluster of cells adjacent to the afferent and efferent blood vessels of the renal corpuscle. As the nephrons are filtering blood, juxtaglomerular cells monitor blood pressure. If they detect a decrease in pressure, they release the hormone renin into the bloodstream.
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...
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: 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,...
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...