The adipose renin–angiotensin system: Role in cardiovascular disease

Several reviews have highlighted the importance of local tissue production of components of the renin–angiotensin system (RAS) [Bader, M., Ganten, D., 2008. Update on tissue renin–angiotensin systems. J. Mol. Med. 86, 615–621; Krop, M., Danser, A.H., 2008. Circulating versus tissue renin–angiotensin system: on the origin of (pro)renin. Curr. Hypertens. Rep. 10, 112–118; Paul, M., Poyan Mehr, A., Kreutz, R., 2006. Physiology of local renin–angiotensin systems. Physiol. Rev. 86, 747–803]. While the concept of tissue RAS is gaining more widespread acceptance, the concept of local angiotensin II (AngII) production, acting in coordinate or independently of the endocrine RAS, continues to be debated. The primary reasons that local AngII production has been studied by many investigators are that components of the RAS are expressed by multiple cell types, and that the endocrine RAS cannot fully explain all effects of AngII. Moreover, through the development and study of genetically altered models for over-expression or knockdown of individual RAS components within specific cell types, it is becoming increasingly more evident that local RAS contribute to effects of AngII in normal physiology and disease. The purpose of this review is to define the presence and physiological significance of a local RAS in adipose tissue in relation to cardiovascular disease.