Related Experiment Video

Updated: Aug 9, 2026

Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents
10:53

Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents

Published on: July 3, 2013

1,25(OH)2D3 suppresses expression and secretion of atrial natriuretic peptide from cardiac myocytes

J Wu1, M Garami, L Cao

  • 1Department of Medicine, University of California, San Francisco 94143, USA.

The American Journal of Physiology
|June 1, 1995
PubMed

Insights

1,25-dihydroxyvitamin D3 (1,25(OH)2D3) inhibits atrial natriuretic peptide (ANP) gene expression and secretion in heart cells. This vitamin D effect on cardiovascular function may involve retinoic acid receptor interactions.

Area of Science:

  • Cardiovascular Physiology
  • Molecular Endocrinology
  • Gene Regulation

Background:

  • Atrial natriuretic peptide (ANP) plays a crucial role in cardiovascular homeostasis.
  • Vitamin D metabolites, including 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], are increasingly recognized for their systemic effects.
  • The specific impact of 1,25(OH)2D3 on cardiac ANP regulation requires further elucidation.

Purpose of the Study:

  • To investigate the effects of 1,25(OH)2D3 on rat atrial natriuretic peptide (ANP) gene expression and secretion.
  • To explore the underlying molecular mechanisms, including potential interactions with retinoic acid signaling.
  • To determine if these effects are calcium-dependent and if non-calcemic vitamin D analogs exert similar actions.

Main Methods:

  • Primary neonatal rat cardiac myocyte cultures were utilized.
  • Cells were treated with varying doses and durations of 1,25(OH)2D3, with and without retinoic acid.
  • ANP secretion, ANP mRNA levels, and ANP gene transcription rates were quantified.
  • Experiments were conducted under both standard and calcium-depleted conditions.

Main Results:

  • 1,25(OH)2D3 demonstrated a dose- and time-dependent inhibition of agonist-stimulated ANP secretion.
  • This inhibition correlated with reduced ANP mRNA transcript levels, indicating transcriptional suppression.
  • Co-treatment with retinoic acid amplified the suppressive effects on ANP mRNA and transcription, suggesting receptor heterodimerization.
  • A non-calcemic analog, 22-oxacalcitriol, mimicked these inhibitory effects, independent of calcium levels.

Conclusions:

  • 1,25(OH)2D3 significantly suppresses ANP gene expression and secretion in cardiac myocytes.
  • The mechanism likely involves direct suppression of ANP gene transcription, potentially mediated by interactions between vitamin D and retinoic acid receptors.
  • These findings highlight a novel role for vitamin D in regulating cardiovascular function, independent of its calcium-modulating effects.

More Related Videos

Isolation of Atrial Myocytes from Adult Mice08:34

Isolation of Atrial Myocytes from Adult Mice

Published on: July 25, 2019

Simultaneous Isolation and Culture of Atrial Myocytes, Ventricular Myocytes, and Non-Myocytes from an Adult Mouse Heart11:53

Simultaneous Isolation and Culture of Atrial Myocytes, Ventricular Myocytes, and Non-Myocytes from an Adult Mouse Heart

Published on: June 14, 2020

Related Concept Videos

Transducer Mechanism: Enzyme-Linked Receptors01:27

Transducer Mechanism: Enzyme-Linked Receptors

Enzyme-linked receptors are cell-surface receptors acting as an enzyme or associating with an enzyme intracellularly. They make excellent drug targets. Drugs can bind to the extracellular ligand-binding domain or directly affect their enzymatic domain and alter their activity.
Major types that are helpful drug targets include:
Adrenergic Receptors: β Subtype01:26

Adrenergic Receptors: β Subtype

β-adrenoceptors have varied sensitivities towards adrenaline, noradrenaline, and isoprenaline. The order of agonist potency is as follows:
Isoprenaline > Adrenaline > Noradrenaline
Neurotransmitter binding to these receptors causes activation of adenylyl cyclase resulting in increased concentrations of cAMP and modulation of calcium ion channels within the cell. They are further classified into β1, β2, and β3 subtypes.
β1-adrenoceptors: β1-adrenoceptors have equal affinities for...
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: 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,...
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...
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...