Angiotensin II increases intracellular Ca2+ in a subpopulation of neurons acutely dissociated from the nucleus of the solitary tract of adult rats

Angiotensin II (AngII) increases intracellular Ca2+ ([Ca2+]i) in neuroblastoma Neuro‐2A cells (Hypertension 45:717, 2005). The goal of this study was to determine if AngII increases [Ca2+]i in neurons in the nucleus of the solitary tract (NTS). NTS neurons from 1–3 month old rats were enzymatically dispersed and loaded with fura‐2AM (2μM). [Ca2+]i was measured before and after AngII (5μM) and cells which did not respond to AngII were tested with the Ca2+ ionophore ionomycin (5μM) to ensure correct placement of the drug delivery pipette and cell viability. Out of a total of 99 cells studied, 62 neurons were excluded from analysis because they did not respond to AngII and ionomycin or their resting [Ca2+]i was more than 250nM. Ionomycin increased [Ca2+]i to 965±227nM (n=29). Resting [Ca2+]i levels were no different in AngII‐responsive (113±17nM, n=11) and AngII‐nonresponsive neurons (125±8nM, n=26). In the 11 NTS neurons that responded to AngII application, AngII increased [Ca2+]i to 289±66nM (p≤.01 compared to resting [Ca2+]i). AngII‐induced increases in [Ca2+]i were eliminated by co‐ application of AT1 receptor antagonist losartan (20μM, n=3). Not all NTS neurons respond to AngII with an increase in [Ca2+]i. This may explain the observation that 50% of NTS neurons respond to AngII with a post‐synaptic depolarization and in the other 50% AngII increases excitatory transmitter release ( Am J Physiol , 284 :, 2003).