ABSTRACT
The renin-angiotensin-aldosterone system (RAAS) is related to dysfunctional adipose tissue, but the actions of angiotensin II (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 (10-17 M to 10-6 M) and noradrenaline (NOR - 10-10 M to 10-4 M) in presence or not of antagonists (Losartan Potassium 10-4 M, 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 10-7 M 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.
Subject(s)
Adipocytes/metabolism , Angiotensin II/pharmacology , Cell Separation , Glycolysis/drug effects , Lipolysis/drug effects , Renin-Angiotensin System/drug effects , Adipocytes/drug effects , Animals , Area Under Curve , Epididymis/cytology , Male , Rats, Inbred SHR , Rats, Inbred WKYABSTRACT
There is a lack of information correlating low adiposity with hypertension experienced by Spontaneous Hypertensive Rats (SHR) or overweight and normotension in Wistar-Kyoto (WKY). We aimed to investigate this lipodystrophy phenomenon by measuring fluorescence lifetime (FLIM), optical redox ratio (ORR), serum levels of hypothalamic-pituitary-adrenal (HPA) and/or hypothalamic-pituitary-thyroid (HPT) hormones axes between Wistar, WKY and SHR before and after establishment of hypertension. Under high blood pressure, we evaluated serum adipokines. Brown adipose tissue was characterized as lower ORR and shorter FLIM compared to white adipose tissue. HPT axis showed a crucial role in the SHR adipose tissue configuration by attenuating whitening. The increased adiposity in WKY may act as a preventive agent for hypertension, since SHR, with low adiposity, establishes the disease. The hypertensive environment can highlight key adipokines that may result in new therapeutic approaches to the treatment of adiposity dysfunctions and hypertension.