AIM:Portal hypertension is a common complication ofliver cirrhosis.Intrahepatic pressure can be elevatedin several ways.Abnormal architecture affectingthe vasculature,an increase in vasoconstrictors andincreased circulation from the splanchnic viscera intothe portal system may all contribute.It follows thatendogenous vasodilators may be able to alleviate thehypertension.We therefore aimed to investigate thelevels of endogenous vasodilators,nitric oxide(NO)andcarbon monoxide(CO)through the expression of nitricoxide synthase(NOS)and heme oxygenase(HO).METHOD:Cirrhotic(n=20)and non-cirrhotic(n=20)livers were obtained from patients whohad undergone surgery.The mRNA and proteinexpressions of the various isoforms of NOS and HOwere examined using competitive PCR,Western Blot andimmunohistochemistry.RESULTS:There was no significant change in eitherinducible NOS(iNOS)or neuronal NOS(nNOS)expressions while endothelial NOS(eNOS)was up-regulated in cirrhotic livers.Concomitantly,caveolin-1,anestablished down-regulator of eNOS,was up-regulated.Inducible HO-1 and constitutive HO-2 were found toshow increased expression in cirrhotic livers albeit indifferent localizations.CONCLUSION:The differences of NOS expressionmight be due to their differing roles in maintaining liverhomeostasis and/or involvement in the pathology ofcirrhosis.Sheer stress within the hypertensive liver mayinduce increased expression of eNOS.In turn,caveolin-1 is also increased.Whether this serves as a defensemechanism against further cirrhosis or is a consequenceof cirrhosis,is yet unknown.The elevated expressionof HO-1 and HO-2 suggest that CO may compensatein its role as a vasodilator albeit weakly.It is possiblethat CO and NO have parallel or coordinated functionswithin the liver and may work antagonistically in thepathophysiology of portal hypertension. AIM: Portal hypertension is a common complication of liver cirrhosis. Intrahepatic pressure can be elevated in several ways. Abnormal architecture affects the vasculature, an increase in vasoconstrictors and increased circulation of the splanchnic viscera intothe portal system may all contribute. It can be able to alleviateiate thehypertension.We therefore aimed to investigate the levels of endogenous vasodilators, nitric oxide (NO) andcarbon monoxide (CO) through the expression of nitricoxide synthase (NOS) and heme oxygenase (HO) .METHOD: Cirrhotic (n = 20) and non-cirrhotic (n = 20) livers were obtained from patients who underdone surgery. The mRNA and proteinexpressions of the various isoforms of NOS and HOwe examined by competitive PCR, Western Blot and immunohistochemistry. RESULTS: There was no significant change in eitherinducible NOS (iNOS) or neuronal NOS (nNOS) expressions while endothelial NOS (eNOS) was up-regulated in cirrhotic livers. Confitantly, caveolin-1, anestab lished down-regulator of eNOS, was up-regulated. Inducible HO-1 and constitutive HO-2 were found toshow increased expression in cirrhotic livers albeit indifferent localizations. CONCLUSION: The differences of NOS expression might be due to their differing roles in maintaining liver homeostasis and / or involvement in the pathology of cirrhosis. heer stress within the hypertensive liver mayinduce increased expression of eNOS. turn, caveolin-1 is also increased. Hether this serves as a defense mechanism of further cirrhosis or is a consequence of cirrhosis, is yet unknown. elevated expressionof HO-1 and HO-2 suggest that CO may compensate in its role as a vasodilator albeit weakly. It is possible that the CO and NO have parallel or coordinated functions with the liver and may work antagonistically in the pathophysiology of portal hypertension.