The renin-angiotensin system (RAS) is involved in nerve regeneration and inflammation; therefore, its potential therapeutic effects have been evaluated in these fields. Most available drugs affect the system through the activity of type 1 and 2 angiotensin II receptors (AT1R & AT2R). However, little is known about how the bioavailability of these receptors changes in response to inflammation or by their pharmacological manipulation. We sought to evaluate the bioavailability of these receptors in these two contexts via a controlled in vitro approach. In primary cultures of postnatal rat dorsal root ganglion cells, we administered different treatments: inflammatory soup (IS), angiotensin-II (AngII), Azilsartan (AT1R-antagonist), or PD123319 (AT2R-antagonist) and examined 2 culture durations (2 or 3 days in vitro, DIV). Cultures were analyzed by qRT-PCR, WB and immunostaining. The addition of AngII to cultures increased the expression of both receptors at 2DIV. PD123319 reduced the levels of both receptors, while Azilsartan prevented only the increase in AT2R in neurons identified by β-tub III. Moreover, IS alone increased the levels of AT1R and AT2R in neurons. Conversely, at 2DIV, treatment with AngII, acting through both receptors, decreased the expression of pro-inflammatory receptors for IL6 and TNFα. Thus, we conclude that the RAS system components interact with each other and with inflammatory components, regulating their availability in a time-dependent manner.