The renin-angiotensin-aldosterone system (RAAS) is related to dysfunctional adipose tissue, but the actions of AII in adipocytes remains unclear. This study aimed to investigate the effects of RAAS blockers and AII in lipolysis and glycolysis from isolated adipocytes in Wistar (WIS), Wistar-Kyoto (WKY) and Spontaneously Hypertensive Rats (SHR). Adipocytes from 15-weeks-old WIS, WKY and SHR were incubated with AII (10^-17M to 10^-6M) and noradrenaline (NOR - 10^-10M to 10^-4M) in presence or not of antagonists (Losartan Potassium 10-4M, PD 123319 5.6 nM or co-incubation). Glycerol and lactate production in WIS and WKY were not affected by the RAAS blockade. SHR glycerol was attenuated by the blockers but lactate was not affected. NOR induced increase in glycerol from 10^-7M for all strains. Normotensive rats are not affected by blockers but decreased lipolytic activity ins SHR. The SHR hypolipodistrophy cannot be related to any disturbance in lipolytic or glycolytic upstream pathways.

肾素-血管紧张素-醛固酮系统 (RAAS) 与功能失调的脂肪组织有关，但 AII 在脂肪细胞中的作用仍不清楚。本研究旨在研究 RAAS 阻滞剂和 AII 在来自 Wistar (WIS)、Wistar-Kyoto (WKY) 和自发性高血压大鼠 (SHR) 的分离脂肪细胞的脂解和糖酵解中的影响。来自 15 周龄 WIS、WKY 和 SHR 的脂肪细胞与 AII（10 ^-17 M 至 10 ^-6 M）和去甲肾上腺素（NOR - 10 ^-10 M 至 10 ^-4M) 存在或不存在拮抗剂（氯沙坦钾 10-4M，PD 123319 5.6 nM 或共孵育）。WIS 和 WKY 中的甘油和乳酸产量不受 RAAS 封锁的影响。SHR 甘油被阻滞剂减弱，但乳酸不受影响。对于所有菌株，NOR 诱导甘油从 10 ^-7 M增加。血压正常的大鼠不受阻滞剂的影响，但会降低 SHR 中的脂肪分解活性。SHR 低脂血症与脂解或糖酵解上游途径的任何紊乱无关。