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Selective potentiation of N‐type calcium channels by angiotensin II in rat subfornical organ neurones
Author(s) -
Washburn David L. S.,
V. Ferguson Alastair
Publication year - 2001
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.2001.t01-1-00667.x
Subject(s) - subfornical organ , long term potentiation , calcium , angiotensin ii , neuroscience , chemistry , medicine , endocrinology , biology , receptor
1 Here we have characterized Ca 2+ 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 ( V 50 ) of activation −14 mV). Using Ba 2+ as the charge carrier, little inactivation was observed, and it occurred only at depolarized potentials ( V 50 of inactivation −12 mV). More inactivation was observed using Ca 2+ as the charge carrier, indicating that Ca 2+ ‐dependent inactivation plays a role in regulating Ca 2+ channel function in subfornical organ (SFO) neurones. 2 The net Ba 2+ current could be blocked by Cd 2+ (EC 50 1.6 μ m ), confirming that currents are of the HVA variety. By using selective antagonists, we identified the presence of both L‐ and N‐type channels; 20 μ m nifedipine blocked 22 ± 1 % of the current, while ω‐conotoxin GVIA blocked 65 ± 7 %, indicating that these currents make up the net current through Ca 2+ channels. 3 Angiotensin II potentiated the inward current throughout the range of activation. Using depolarizing voltage ramps, 1 n m angiotensin potentiated the peak current by 14 ± 5 %. We then used selective blockade of the HVA component currents; 20 μ m nifedipine failed to prevent the potentiation by angiotensin II (12 ± 5 %), while blocking N‐type channels with ω‐conotoxin GVIA blocked the facilitation by ANG (2.3 ± 2 %). Losartan (1 μ m ) 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 AT 1 receptors.