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- W3168020009 abstract "In rat cerebral arteries, T-type Ca2+ channels are suppressed by protein kinase A (PKA) signaling. In this study, we examine whether protein kinase G (PKG), another key vasodilatory pathway, exerts a similar or distinctive influence on this conductance. Using patch clamp electrophysiology and cerebral arterial smooth muscle cells from rat, we monitored an inward Ba2+ current that was divisible into nifedipine-sensitive and –insensitive components. The nifedipine-insensitive conductance displayed properties reminiscent of T-type Ca2+ channels; faster activation and steady state inactivation particularly at hyperpolarized potentials. Intriguingly, agents that target key PKG signaling proteins altered T-type Ca2+ channel activity. In particular, activators of PKG signaling (db-cGMP, Na nitroprusside, SNAP) suppressed T-type currents and evoked a hyperpolarized shift in steady state inactivation. PKG inhibitors (KT5823, ODQ) masked this suppression while having no effect on basal T-type activity. In contrast, PKG manipulations had no influence on the nifedipine-sensitive L-type conductance. Cumulatively, our findings support the emerging view that T-type Ca2+ channels are a key regulatory target of vasodilatory signaling pathways (i.e. PKG and PKA)." @default.
- W3168020009 created "2021-06-22" @default.
- W3168020009 creator A5068389319 @default.
- W3168020009 creator A5088271995 @default.
- W3168020009 date "2013-04-01" @default.
- W3168020009 modified "2023-09-28" @default.
- W3168020009 title "Protein Kinase G Inhibits T‐type Ca 2+ Channels in Rat Cerebral Arteries" @default.
- W3168020009 doi "https://doi.org/10.1096/fasebj.27.1_supplement.921.3" @default.
- W3168020009 hasPublicationYear "2013" @default.
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