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Comment
. 2011 May;137(5):473-7.
doi: 10.1085/jgp.201110607. Epub 2011 Apr 11.

Interaction between IP₃ receptors and BK channels in arterial smooth muscle: non-canonical IP₃ signaling at work

Patricio E Mujica  1 , Francisco G González
Affiliations
Comment

Interaction between IP₃ receptors and BK channels in arterial smooth muscle: non-canonical IP₃ signaling at work

Patricio E Mujica et al. J Gen Physiol. 2011 May.
No abstract available

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Figures

Figure 1.
Figure 1.
IP3-induced interactions between IP3Rs and ion channels in arterial SMCs. Induction of Ca2+ release from the SR via IP3R (solid orange arrows) is the best-known mechanism of action of IP3. Non-canonical IP3 signaling is independent of SR Ca2+ release and involves an IP3-induced interaction of IP3R1 with plasma membrane channels such as TRPC3 and BKCa (red arrowheads), possibly localized in membrane caveolae. TRPC3 activation by IP3R1 induces a nonselective cation current (ICat; solid green arrow) that depolarizes the cell membrane, activating VDCC and BKCa channels (dashed green arrows). BKCa channels are also activated by Ca2+ (dashed orange arrows). Whereas VDCCs mediate Ca2+ influx through the plasma membrane (purple arrow) leading to contraction, K+ efflux through BKCa channels (blue arrow) leads to hyperpolarization of the cell membrane, which closes VDCCs, leading to SMC relaxation.
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