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See related article, pp 1524–1530 Adipose tissue has classically been assumed to function simply as a depot storing excess metabolic fuels that can be mobilized during energy deprivation. It is now well recognized, however, that adipocytes are major players in the regulation of a large number of physiological functions including blood pressure.1 Among ways, adipocytes influence physiological processes; it is arguably their ability to produce and secrete hormones that act in a paracrine or endocrine fashion that has reinvigorated the study of this cell type. For instance, adipocyte-derived angiotensinogen (AGT), the only known precursor of angiotensin II (Ang II), is known to contribute to the circulating pool of this protein.1–6 In the current issue of Hypertension , Yiannikouris et al7 describe a new way by which fat can affect the circulating renin-angiotensin system (RAS) and blood pressure.The realization that essentially all components of the RAS are expressed in adipose tissue led to the notion of a local adipose RAS that may influence metabolism as well as blood pressure.2 This was further supported by studies in humans showing positive correlations among fat mass, circulating AGT, and RAS activity3 that are reversible by weight loss.4 The relevance of the local adipose RAS to blood pressure control was established …

The Adipose/Circulating Renin-Angiotensin System Cross-Talk Enters a New Dimension