Regular paperWhole cell patch recordings from forebrain slices demonstrate angiotensin II inhibits potassium currents in subfornical organ neurons
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Cited by (43)
Mechanisms of GABA-mediated inhibition of the angiotensin II-induced cytosolic Ca<sup>2+</sup> increase in rat subfornical organ neurons
2021, Brain ResearchCitation Excerpt :The inhibitory action of galanin in other areas of the brain, such as the locus coeruleus and supraoptic nucleus neurons, is thought to be due to increased K+ conductance across the cell membrane (Papas and Bourque, 1997; Ren et al., 2001). AII suppresses outward-rectifying K+ current in SFO neurons (Ferguson and Li, 1996); therefore, it is possible that galanin hyperpolarizes the cell membrane and suppresses SFO neuronal activation by opening K+ channels which were closed by AII or other K+ channels on which AII did not act. As we found that the AII-induced persistent [Ca2+]i increase has voltage-dependent component (Izumisawa et al., 2019b); the inhibition by galanin may be explained, at least in part, by the above-mentioned effects on K+ channels.
Persistent cytosolic Ca<sup>2+</sup> increase induced by angiotensin II at nanomolar concentrations in acutely dissociated subfornical organ (SFO)neurons of rats
2019, Brain ResearchCitation Excerpt :The former is independent of CaMK, while the latter is dependent on phosphorylation by CaMK. The initial phase thus may be explained by the reported actions of AT1 receptor activation, such as non-selective cation channel activation, K+ channel inhibition and Ca2+ channel potentiation (Ferguson and Li, 1996; Wang et al., 2013; Washburn and Ferguson, 2001). CaMK is a multifunctional protein kinase and highly expressed in central nervous system neuronal cells.
The cytosolic Ca<sup>2+</sup> concentration in acutely dissociated subfornical organ (SFO) neurons of rats: Spontaneous Ca<sup>2+</sup> oscillations and Ca<sup>2+</sup> oscillations induced by picomolar concentrations of angiotensin II
2019, Brain ResearchCitation Excerpt :However, the result that extracellular Ca2+ removal inhibited AII-induced Ca2+ increases clearly indicates that voltage-dependent Ca2+ entry is the major source of the [Ca2+]i increase in response to AII in SFO neurons. AII can activate voltage-dependent Ca2+ entry in two ways: activation of non-selective cation channels (Ono et al., 2001) and inhibition of the outwardly rectifying K+ currents (Ferguson and Li, 1996). The findings that AII-induced Ca2+ oscillations were susceptible to inhibition by Ca2+ removal, Na+ replacement, and TTX, as were spontaneous Ca2+ oscillations, suggest that a common mechanism underlies the two Ca2+ oscillations.
Circumventricular organs: Targets for integration of circulating fluid and energy balance signals?
2013, Physiology and BehaviorCitation Excerpt :It is also interesting to note the expression levels of AT1 receptors in the SFO have been reported to be decreased in hypertensive states [46], thus highlighting the dynamic nature of angiotensin II effects on SFO neurons in accordance with the cardiovascular status of the organism. Finally, patch-clamp recordings have revealed that angiotensin II modulates numerous conductances to exert its central effects, namely by inhibiting the transient potassium conductance IA [47], and potentiating both a non-selective cation conductance [48] and voltage-gated calcium channels [49]. Since these studies demonstrating SFO neurons to be critical sensors of circulating angiotensin II, considerable additional evidence has highlighted roles for this CVO in responding to many other circulating signals of importance to cardiovascular regulation and fluid balance.
AT2 receptor signaling and sympathetic regulation
2011, Current Opinion in Pharmacology