Endothelins as mediators in the modulation of cardiac performance

Smiljic, Sonja; Radovic, Dragica; Nestorović, Vojkan; Milanovic, Zvezdan; Biševac, B.

doi:10.5937/pramed1404079s

Cited by 2 publications

(1 citation statement)

References 22 publications

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“…Adding a mediator of endothelial origin will not restore or prevent the loss of heart contractility. The EE can affect the establishment of transcellular physicochemical gradient across the endocardium, and thereby affects the cardiac function [6].…”

Section: Introductionmentioning

confidence: 99%

Endocardial endothelium as a blood-heart barrier

et al. 2018

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Introduction. Endocardial endothelium is formed from a single layer of closely related cells with complex interrelationships and extensive overlap at the junctional edges. Morphological characteristics of blood-heart barrier. Endocardium is composed of three layers: endocardial endothelium, subendothelial loose connective tissue and subendocardium. The fibrous component of the subendothelium consists of small amount of collagen and elastic fibers. Several cell types are present in subendocardium: telocytes, fibroblasts and nerve endings. Intercellular bonds between the endocardial endothelial cells. Endocardial endothelial cells are attached to one another via sets of binding proteins forming solid, adherent and communicating connections. Communicating connections form transmembrane channels between the neighboring cells, while solid and adherent connections form pericellular structures like stitches. The maintenance of the presumed transendocardial electrochemical potential difference provides a high gradient for certain ions as well as a selective boundary barrier, basal lamina, preventing ionic leakage. The negatively charged glycocalyx also modulates endothelial permeability. Electrophysiological characteristics of heart-blood barrier. Electrophysiological studies have shown the existence of a large number of membrane ion channels in the endocardial endothelial cells: inward rectifying K + channels, Ca 2+ dependent K + channels, voltage-dependent Clchannels, volume-activated Clchannels, stretch-activated cation channels and one carrier mediated transport mechanism-Na + K + adenosine triphosphatase. Conclusion. Numerous diseases of the cardiovascular system may be a consequence, but also the cause of the endocardial endothelium dysfunction. Selective damage to the endocardial endothelium and subendocardium is found in arrhythmia, atrial fibrillation, ischemia/reperfusion injury and heart failure. Typical lesions of endocardial and microvascular endothelium have also been described in sepsis, myocardial infarction, inflammation and thrombosis. The result of endothelial dysfunction is the weakening of the endothelial barrier regulation and electrolyte imbalance of the subendocardial interstitium.

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Section: Introductionmentioning

confidence: 99%

Endocardial endothelium as a blood-heart barrier

et al. 2018

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The clinical significance of endocardial endothelial dysfunction

Smiljic¹

2017

Medicina

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Endocardial endothelium (EE) is essential in the embryonic development of the heart, the optimal contractility and rhythm as well as the remodeling of the heart. Endocardial endothelium affect the contractility of cardiomyocytes through paracrine signaling substances such as nitric oxide (NO), endothelin (ET-1), prostaglandins (PGI2, PGF2, PGE2) and angiotensin II (ANG II). Typical lesions of endocardial endothelium have been described in atrial fibrillation, ischemia/reperfusion injury, cardiac hypertrophy, heart failure, sepsis, myocardial infarction, inflammation and thrombosis. In patients with atrial fibrillation, there can be a systemic endothelial dysfunction that combines endocardial and vascular endothelial dysfunction and leads to increased hemodynamic load of the left atrium and increased synthesis and release of natriuretic peptides, angiotensin II, aldosterone and growth factors from the atrial myocardium. A dysfunction of endothelial cells in the local inflammatory status can lead to increased plaque vulnerability, which contributes to plaque rupture and favors the formation of thrombus. Preserving the endocardial-myocardial integrity plays a significant role in the prevention of a coronary artery disease. Endocardial endothelial dysfunction is, similarly to coronary endothelial dysfunction, an early event that leads to the progression of heart failure. Multimarker strategy, that would include a different set of biomarkers, could significantly help in the assessment of patients with cardiovascular diseases. The challenge lays in finding new therapeutic strategies that would, by preserving endothelial function, prevent the onset of cardiovascular diseases.

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Endothelins as mediators in the modulation of cardiac performance

Cited by 2 publications

References 22 publications

Endocardial endothelium as a blood-heart barrier

Endocardial endothelium as a blood-heart barrier

The clinical significance of endocardial endothelial dysfunction

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