Related Experiment Video

Updated: Jul 8, 2026

Assessment of Vascular Tone Responsiveness using Isolated Mesenteric Arteries with a Focus on Modulation by Perivascular Adipose Tissues
08:41

Assessment of Vascular Tone Responsiveness using Isolated Mesenteric Arteries with a Focus on Modulation by Perivascular Adipose Tissues

Published on: June 3, 2019

[Effects of endotheline and nitric oxide on vascular tonicity in patients with chronic cardiac failure]

E N Denisov, Ia I Kots, R Z Bakhtiiarov

    Terapevticheskii Arkhiv
    |January 29, 2008
    PubMed

    Insights

    Chronic cardiac failure (CCF) impairs vascular tone regulation due to altered endothelin-1 (ET-1) and nitric oxide (NO) metabolism. These changes worsen with CCF severity, impacting tissue oxygenation.

    Area of Science:

    • Cardiovascular Physiology
    • Endothelial Function
    • Vascular Biology

    Background:

    • Chronic cardiac failure (CCF) affects vascular tonicity regulation.
    • Endothelium-dependent mechanisms are crucial for maintaining vascular tone.
    • The roles of endothelin-1 (ET-1) and nitric oxide (NO) in CCF are not fully understood.

    Purpose of the Study:

    • To investigate the effects of ET-1 and NO on endothelium-dependent vascular tonicity regulation in CCF patients.
    • To correlate these effects with the severity of CCF (FC I-IV).

    Main Methods:

    • Vascular reactions assessed using high-resolution ultrasound (D.S. Celermajer method).
    • Tissue oxygenation measured by transcutaneous polarography.
    • Endothelial NO-synthase expression, NO metabolites, and ET-1 levels analyzed.

    Main Results:

    • CCF patients exhibit reduced endothelium-dependent vascular reactions.
    • These vascular dysfunctions progress with increasing CCF severity.
    • Altered metabolism of ET-1 and NO contributes to these disorders.

    Conclusions:

    • CCF is associated with impaired endothelium-dependent vascular tonicity regulation.
    • Disturbed ET-1 and NO metabolism, linked to abnormal tissue oxygenation, underlies these changes.
    • The severity of CCF dictates the extent of these endothelial dysfunction mechanisms.
    Abstract

    More Related Videos

    Assessment of Vascular Function in Patients With Chronic Kidney Disease08:50

    Assessment of Vascular Function in Patients With Chronic Kidney Disease

    Published on: June 16, 2014

    Assessing Endothelial Vasodilator Function with the Endo-PAT 200007:46

    Assessing Endothelial Vasodilator Function with the Endo-PAT 2000

    Published on: October 15, 2010

    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...
    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...
    Heart Failure V: Medical Management01:30

    Heart Failure V: Medical Management

    Medical Management of Acute Decompensated Heart Failure (ADHF)The primary goals of therapy for patients hospitalized with acute decompensated heart failure (ADHF) include:Relieving symptomsOptimizing volume statusSupporting oxygenation and ventilationMaintaining cardiac output (CO) and end-organ perfusionIdentifying and addressing the cause of ADHFPreventing complicationsProviding patient education on factors precipitating HF exacerbationPlanning for dischargeOngoing monitoring and assessment...
    Heart Failure Drugs: Inotropic Agents01:26

    Heart Failure Drugs: Inotropic Agents

    Positive inotropic agents are commonly used as the first line of treatment for heart failure. One such agent is digoxin, derived from the genus Digitalis, which has been known for centuries but effectively utilized since 1785. However, these cardiac glycosides can have potentially toxic effects due to their mechanism of action, which involves inhibiting Na+/K+-ATPase and increasing contractility. Digoxin is absorbed orally and distributed in various tissues, including the CNS. It has a long...
    Heart Failure Drugs: Diuretics01:22

    Heart Failure Drugs: Diuretics

    Heart failure and kidney perfusion are interconnected in a complex way. Reduced renal perfusion and venous congestion are two significant factors that contribute to renal dysfunction in heart failure. The kidneys, primarily responsible for fluid balance in the body, are adversely affected due to compromised cardiac output and increased venous pressure. In response to reduced renal perfusion, the kidneys activate neurohumoral mechanisms to restore balance. However, these mechanisms can be...
    Heart Failure VI: Adjunct Therapies01:22

    Heart Failure VI: Adjunct Therapies

    Additional therapies for treating patients with heart failure (HF) may include procedural interventions, supplemental oxygen, the management of sleep disorders, and nutritional therapy.Procedural InterventionsImplantable Cardioverter-Defibrillator: For patients at risk of life-threatening arrhythmias due to severe left ventricular dysfunction, an Implantable Cardioverter-Defibrillator (ICD) can detect and terminate these arrhythmias, preventing sudden cardiac death and improving survival rates.