Key result
Hepatic venous PRA is ~26% lower than incoming blood, indicating hepatic extraction of circulating renin.
Why the study?
The role of the human liver in extracting circulating renin and its impact on plasma renin activity was not well established.
Observational (n=8)
The human liver extracts circulating renin, suggesting that elevated plasma renin activity in cirrhosis may be partly due to impaired hepatic inactivation.
Answers are grounded in this paper and cite their sources.
May explain hyperreninemia in cirrhosis; extends animal data to humans yet leaves open quantitative role.
In eight studies, the plasma renin activity (PRA) was determined in blood drawn consecutively from the hepatic vein, a peripheral vessel, and renal veins. The renal venous PRA was consistently higher than the arterial PRA, indicating renal secretion of renin. In seven of the eight studies, hepatic venous PRA was, on the average, 26% lower than the PRA of blood entering the liver indicating hepatic extraction of circulating renin. That the elevated PRA seen in cirrhosis of the liver may in part be related to impared hepatic inactivation of renin is an hypothesis that merits further study.
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Christlieb et al. (1968) reported an observational. Blood passage through the liver vs. Blood entering the liver was evaluated on Plasma renin activity (PRA) (26% lower). Hepatic venous plasma renin activity was on average 26% lower than that of blood entering the liver, indicating hepatic extraction of circulating renin.
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