Figure 1.

Hypothesized mechanisms of metabolic dysfunction via inappropriate cardiac natriuretic peptide feedback among HIV-infected individuals. HIV-infected individuals with a clinical phenotype of excessive adiposity demonstrate increased aldosterone during an RAAS-activated state. BNP is a negative regulator of RAAS. Dysfunctional adipose tissue is highly inflamed and may be linked to upregulation of NPR-C. When bound to NPR-C, BNP is degraded and cleared. Relatively lower BNP may permit an exaggerated increase in aldosterone and could be detrimental to preventing metabolic dysfunction. Appropriate BNP response among individuals with healthy adipose tissue may contribute to maintenance of metabolic homeostasis through physiologic suppression of aldosterone. Triangular structures represent NPR-C and star-like structures represent the inflammatory milieu.