Increased enzymatic activity of renin and hyperlipidemia.
We have previously reported that the in vitro enzymatic activity of exogenous renin, plasma renin reactivity (PRR), is increased in plasma of patients with chronic renal failure, possibly due to the deficiency of a renin inhibitor. To determine whether increases PRR is related to renal failure per se or to hyperlipidemia, PRR was measured in 10 control subjects, 10 patients with renal failure, and 10 hyperlipidemic patients with normal renal function. Compared to that in control subjects (52.6 ng angiotensin I generated per ml/h +/- 3.8 SE) PRR was increased (P < 0.05) in plasma of uremic patients (65.1 +/- 4.3) and hyperlipidemic patients (71.4 +/- 10.7). Renin substrate concentration did not differ among groups, and after denaturation of endogenous substrate by acidification of plasma, PRR was still increased. A "protein-free" extract of plasma from normal subjects inhibited renin, whereas little or no inhibition occurred with a comparable extract from uremic patients and hyperlipidemic patients. Thus, alterations in lipid metabolism may account for the increased enzymatic activity of renin in uremic plasma. Increased PRR may be related to the deficiency of a normally occurring renin inhibitor.
D000803:Angiotensin I / Q000097:blood; D002784:Cholesterol / Q000097:blood; D006801:Humans; D006949:Hyperlipidemias / Q000201:enzymology*; D007676:Kidney Failure, Chronic / Q000201:enzymology; D012083:Renin / Q000097:blood*; D014280:Triglycerides / Q000097:blood
D014280:Triglycerides; D000803:Angiotensin I; D002784:Cholesterol; D012083:Renin