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Selective potentiation of N-type calcium channels by angiotensin II in rat subfornical organ neurones

David L. S. Washburn and Alastair V. Ferguson

1. Here we have characterized Ca²⁺ currents in rat subfornical organ neurones, and their modulation by angiotensin II. Currents were of the high voltage-activated (HNA) subtype, as the threshold for activation was near -30 mV (mid-point potential (V₅₀) of activation -14 mV). Using Ba²⁺ as the charge carrier, little inactivation was observed, and it occurred only at depolarized potentials (V₅₀ of inactivation -12 mV). More inactivation was observed using Ca²⁺ as the charge carrier, indicating that Ca²⁺-dependent inactivation plays a role in regulating Ca²⁺ channel function in subfornical organ (SFO) neurones.
2. The net Ba²⁺ current could be blocked by Cd²⁺ (EC₅₀ 1.6 µM), confirming that currents are of the HVA variety. By using selective antagonists, we identified the presence of both L- and N-type channels; 20 µM nifedipine blocked 22 ± 1 % of the current, while -conotoxin GVIA blocked 65 ± 7 %, indicating that these currents make up the net current through Ca²⁺ channels.
3. Angiotensin II potentiated the inward current throughout the range of activation. Using depolarizing voltage ramps, 1 nM angiotensin potentiated the peak current by 14 ± 5 %. We then used selective blockade of the HVA component currents; 20 µM nifedipine failed to prevent the potentiation by angiotensin II (12 ± 5 %), while blocking N-type channels with -conotoxin GVIA blocked the facilitation by ANG (2.3 ± 2 %). Losartan (1 µM) prevented the actions of ANG on the inward current (1.6 ± 1 %), indicating that the selective effects of ANG on N-type channels in SFO neurones are mediated by AT₁ receptors.

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