Sajad Papi
1, Fariba Ahmadizar
2, Amin Hasanvand
3* 1 Department of Pharmacology and Toxicology, Faculty of Pharmacy, Lorestan University of Medical Sciences, Khorramabad, Iran
2 Department of Epidemiology, Erasmus University Medical Center, Rotterdam, Netherlands
3 Hepatitis Research Center, Department of Pharmacology and toxicology, Faculty of Pharmacy, Lorestan University of Medical Sciences, Khorramabad, Iran
Abstract
Nitric oxide (NO) is one of the most important components of blood vessels’ health. NO is a gas compound
with different physiological and biochemical effects on the body. It is a free radical, which plays as an
endogenous and endothelium relaxing factor. NO has a protective role in digestive system which also plays
different roles in the immune system as a mediator of immunity; e.g. regulating immune response, and
stimulation and suppression of the immune system. NO has three isoforms each of which is expressed by
a special gene. These isoforms include neuronal nitric oxide synthase (nNOS) and endothelial nitric oxide
synthase (eNOS) which both are depending on calcium and calmodulin. The third isoform, independent on
calcium and calmodulin, is inducible nitric oxide synthase (iNOS). Even in special conditions such as renal
ischemia-reperfusion, it has been shown that high iNOS and low eNOS levels are involved in increased
inflammation and connective tissue damage.