Could the absence or malfunction of vascular endothelium precipitate the occurrence of vasospasm?
The obligatory role of the endothelium in relaxations of isolated coronary arteries to acetylcholine is explained by the release by endothelial cells of a labile vasodilator substance(s), endothelium-derived relaxing factor(s). Other neurohumoral mediators can evoke endothelium-dependent relaxations of coronary arteries. Of particular importance from the clinical point of view are thrombin, serotonin and adenine nucleotides. The latter are chiefly responsible for the endothelium-dependent relaxations evoked by aggregating platelets. The absence or the dysfunction of the endothelium may favour the occurrence of vasospasm.
D000227:Adenine Nucleotides / Q000502:physiology; D000818:Animals; D001777:Blood Coagulation; D001808:Blood Vessels / Q000502:physiology*; D002395:Catecholamines / Q000502:physiology; D003329:Coronary Vasospasm / Q000209:etiology*; D004285:Dogs; D004727:Endothelium / Q000502:physiology; D066298:In Vitro Techniques; D009126:Muscle Relaxation; D009131:Muscle, Smooth, Vascular / Q000502:physiology; D010974:Platelet Aggregation; D012701:Serotonin / Q000502:physiology; D014667:Vasopressins / Q000502:physiology
D000227:Adenine Nucleotides; D002395:Catecholamines; D014667:Vasopressins; D012701:Serotonin