Hepatic Clearance of Renin in Canine Experimental Models for Low- and High-Output Heart Failure

• Published in: Circulation research Vol. 24; no. 2; pp. 213 - 219
• Main Authors: Schneider, Edward G, Davis, James O, Robb, Charles A, Baumber, John S
• Format: Journal Article
• Language: English
• Published: United States American Heart Association, Inc 01.02.1969
• Subjects: Animals; Aorta; Arteriovenous Fistula - complications; Dogs; Female; Heart Failure - etiology; Heart Failure - metabolism; Liver - metabolism; Liver Circulation; Renin - blood; Renin - metabolism; Sodium - metabolism; Sulfobromophthalein; Vascular Diseases - complications; Vena Cava, Inferior; Venae Cavae
• ISSN: 0009-7330; 1524-4571
• DOI: 10.1161/01.RES.24.2.213

Hepatic blood flow, hepatic extraction of renin, and hepatic clearance of renin were compared in normal conscious dogs, in dogs with constriction of the thoracic inferior vena cava (as a model of low-output heart failure), and in dogs with an aortic-caval fistula (high-output heart failure). Both “failure” preparations showed marked sodium retention. Renin was measured by methods described previously and expressed as nanograms of angiotensin produced during incubation per milliliter of plasma. Hepatic plasma flow was determined by the sodium sulfobromophthalein method. The dogs with low-output heart failure had a marked reduction in hepatic plasma flow, while those with high-output failure showed no significant change in this flow. Plasma renin was significantly elevated in both models of heart failure. Dogs with low-output failure had an increase (P < .05) in hepatic renin extraction from a normal value of 19.8% to 33.4%, while those with high-output failure showed a decrease in hepatic renin extraction to 11.9% (P < .01). The hepatic clearance of renin in low-output failure (104 ml/ min) was the same as the average normal value of 104 ml/min, while clearance of renin by the liver in high-output failure was reduced to 51 ml/min (P < .001). The data provide evidence that the decreased metabolism of renin contributes substantially to the increased plasma level of renin in experimental high-output heart failure.