Inducible Nitric Oxide Synthase and Inflammatory Diseases

Table 1 Regulatory and anti-inflammatory actions of NO

Tissue Organ	Physiological Action of NO Related to Inflammation	NOS Isoform	Refs.*
Vascular	— Maintains vasodilator tone	eNOS	(239)
endothelium	— Inhibits smooth muscle cell migration and proliferation	eNOS; iNOS eNOS	(240,241)
	— Inhibition of blood cell-vessel wall interactions and adhesion to endothelium		(242)
Blood cells	— Inhibition of platelet adhesion and aggregation, and inhibition of microvascular thrombosis	eNOS; iNOS eNOS	(243,244) (242) (245)
	— Prevents aggregation and adhesion of white cells	iNOS	(9,246)
	— Mediates cytostatic and cytotoxic activity of macrophages for antimicrobial and antitumor defense	iNOS	(247,248) (249)
	— Inhibition of mast cell degranulation
Heart	— Maintains coronary perfusion and regulates cardiac contractility	eNOS	(250,251)
	— Inhibits cardiac contractility (pathology of myocarditis)	iNOS	(252–254)
Lung	— Maintains ventilation/perfusion ratio and regulates bronchociliar motility and mucus secretion		(255,256) (257)
Pancreas	— Modulates endocrine secretion	eNOS, iNOS	(258,259)
Intestinal	— Modulates peristalsis and exocrine secretion	eNOS	(208,260)
system	— Contributes to protection of mucosa		(261,262)

* The quoted references are mostly recent reviews of significant relevance. eNOS, endothelial isoform of nitric oxide synthase (NOS); iNOS, inducible form of NOS; NO, nitric oxide.

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