Table 1. Overview Of Endothelium-Derived Vaso-Active Factors.

Endothelium-derived factors	Physiological effects	Enzymatic source and mechanism of action
Nitric oxide (NO)	• Potent vasodilator	• Synthesised by the enzymes: eNOS, nNOS and iNOS, with eNOS the major endothelial source of NO during physiological conditions
	• Inhibits inflammation, VSMC proliferation and migration, platelet aggregation and adhesion, and leukocyte adhesion
	• Regulates myocardial contractility	• Diffuses from endothelial cells to underlying VSMCs where it binds to soluble guanylyl cyclase, leading to a cascade of events that ultimately result in vascular relaxation
	• Regulates cardiac metabolism
	• Cardioprotective during ischaemia–reperfusion injury
Prostacyclin (PGI2)	• Vasodilatory agent	• Derived from arachidonic acid by cyclooxygenase-2 (COX-2)
	• Inhibits platelet aggregation
Endothelium-derived hyperpolarising factor (EDHF)	• Exerts vasodilatory effects, particularly in small arteries of diameter ≤ 300 μm	• Its identity is still under suspicion with proposed candidates such as potassium ions and hydrogen peroxide
		• Causes relation of VSMCs by means of membrane hyperpolarisation
Endothelin-1 (ET-1)	• A potent vasoconstrictor	• Synthesised by endothelin-converting enzyme
		• Exerts its effects via two receptors: ETA expressed on endothelial cells and ETB on VSMCs. ETA receptors promote vasoconstriction, whereas ETB receptors promote NO production and ultimately reduction in ET-1 production
Thromboxane A (TXA2)	• A potent vasoconstrictor	• Derived from arachidonic acid by COX-1
Angiotensin ll	• A potent vasoconstrictor	• Synthesised by angiotensin converting enzyme
		• Elicits its effects via two receptors: AT1 which promotes vasoconstriction and cell proliferation, and AT2 which antagonises the effects of AT1