Cold-acclimation regulates systemic and tissue renin-angiotensin systems

Previous studies demonstrated cold-acclimation (CA) increased angiotensin II (All) content in interscapular brown adipose tissue (ISBAT). Regulation of systemic and tissue (ISBAT, kidney, liver, lung) renin-angiotensin systems was examined in rats acclimated to cold (4°C) for 7 days. While increases in plasma All were not significant between CA (66 ±12 pg/ml) and control (36 ±9 pg/ml) rats, plasma AIII levels were elevated in CA rats (CA:95 ±24 pg/ml; control:28 ± 8 pg/ml). Plasma renin activity was not different between CA and control rats. The Vmax and Km for renin-like activity were decreased (77% and 63%, respectively) in ISBAT from CA rats. In kidney, the Vmax and Km for renin-like activity were increased (3.6 and 10-fold, respectively) in CA rats. [12iI]AII receptor binding kinetics (Kd, Bmax) were determined in membrane preparations from liver, lung and ISBAT from CA and control rats. The affinity for [1BI]AH binding was not altered in any tissue examined; however, All receptor density increased in liver (3.2-fold) and ISBAT (2.3-fold)'from CA rats. Lung AH receptor density was not altered in CA rats. These results suggest cold acclimation increases activity of the systemic renin-angiotensin system. However, tissue-specific alterations in renin activity and/or AH receptor density were evident in liver, lune, kidney and ISBAT from CA rats.