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Inflammation is thought to play a fundamental role in the pathophysiology of hypertension and heart failure, although the mechanisms for this remain unclear. Proinflammatory cytokines, such as tumor necrosis factor-α (TNF-α), influence the subfornical organ (SFO) to modulate sympathetic activity and blood pressure. The pressor effects of TNF-α in the SFO are partially mediated by angiotensin II (ANG II) receptor type 1 (AT 1 R), and TNF-α is known to potentiate ANG II-induced hypertension. However, the cellular mechanism of the interaction between TNF-α and ANG II/AT 1 R signaling remains unknown. In the present study, we performed Ca 2+  imaging on dissociated SFO neurons in vitro from male Sprague-Dawley rats to determine whether TNF-α modulates ANG II-induced increases in intracellular Ca 2+  in SFO neurons. We first established that a proportion of SFO neurons respond to ANG II, an effect that required AT 1 R signaling and extracellular Ca 2+ . We then tested the hypothesis that TNF-α may modulate the effects of ANG II on SFO neurons by examining the effects of TNF-α treatment on the ANG II-induced rise in intracellular Ca 2+ . We discovered that TNF-α potentiated the ANG II-induced rise in intracellular Ca 2+ , an effect that was dependent on the duration of TNF-α treatment. Finally, we determined that this potentiation of ANG II-induced Ca 2+  activity relied on tetrodotoxin-sensitive voltage-gated Na +  (vgNa + ) channels. These data suggest that the potentiation of ANG II/AT 1 R activity by TNF-α in SFO neurons results from the previously demonstrated ability of this cytokine to modulate the activation threshold of vgNa +  currents.

american journal of physiology. regulatory, integrative and comparative physiology/american journal of physiology. regulatory, integrative, and comparative physiology

Tumor necrosis factor-α potentiates the effects of angiotensin II on subfornical organ neurons