Atrial angiotensin-(1-12)/chymase expression data in patient of heart diseases

Hao Wang1,2, Jasmina Varagic3,4,5, Sayaka Nagata3

  • 1Department of Anesthesiology, Wake Forest School of Medicine, Winston-Salem, NC, USA.

Data in Brief
|June 4, 2020
PubMed

Insights

The angiotensin-(1-12) [Ang-(1-12)]/chymase axis is more active in the left atrium than the right. This axis was further investigated in relation to stroke, heart failure, and atrial fibrillation.

Area of Science:

  • Cardiovascular Biology
  • Biochemistry
  • Human Physiology

Background:

  • The renin-angiotensin system plays a crucial role in cardiovascular homeostasis.
  • Angiotensin-(1-12) [Ang-(1-12)] is a precursor to Angiotensin II, a key effector peptide.
  • Chymase is a serine protease that can generate Angiotensin II from Ang-(1-12).

Purpose of the Study:

  • To investigate the differential expression of the Ang-(1-12)/chymase axis in human atrial tissue.
  • To compare Ang-(1-12) and chymase levels in left versus right atria.
  • To explore the association of atrial Ang-(1-12) and chymase expression with clinical conditions like stroke, heart failure, and atrial fibrillation.

Main Methods:

  • Analysis of chymase gene transcripts and activity in human atrial tissue.
  • Measurement of immunoreactive Ang-(1-12) expression levels.
  • Comparison of these markers between left and right atrial samples.
  • Correlation with echocardiographic data and patient clinical history (stroke, heart failure, postoperative atrial fibrillation).

Main Results:

  • Chymase gene transcripts, activity, and Ang-(1-12) expression were significantly higher in the left atrium compared to the right atrium.
  • These differences persisted irrespective of underlying cardiac disease.
  • Elevated left atrial chymase and Ang-(1-12) levels were observed in patients with specific clinical conditions, warranting further investigation.

Conclusions:

  • The human left atrium exhibits higher expression and activity of the Ang-(1-12)/chymase axis compared to the right atrium.
  • This axis may be implicated in the pathophysiology of conditions such as stroke, heart failure, and atrial fibrillation.
  • Further research is needed to elucidate the precise role of this axis in cardiovascular disease.

Related Concept Videos

Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...
575
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...
800
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...
2.2K
Blood Studies for Cardiovascular System II: CRP, Hcy, and Cardiac Natriuretic Peptide Markers01:19

Blood Studies for Cardiovascular System II: CRP, Hcy, and Cardiac Natriuretic Peptide Markers

Cardiac biomarkers are critical in diagnosing, prognosing, and managing cardiovascular diseases. Routine measurement of specific biomarkers such as B-type natriuretic peptide (BNP), C-reactive protein (CRP), and homocysteine (Hcy) is common practice in clinical settings to evaluate heart function and predict cardiovascular events.
These markers indicate stress or strain on the heart muscle:
Natriuretic Peptides (BNP)
Cardiac myocytes produce these hormones in response to ventricular stretching...
428
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,...
1.1K
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,...
1.8K