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Published on: July 14, 2018
Transient receptor potential (TRP) channels, vascular tone and autoregulation of cerebral blood flow
Joseph E Brayden1, Scott Earley, Mark T Nelson
1Department of Pharmacology, The University of Vermont, 89 Beaumont Avenue, Burlington, VT 05405, USA. joe.brayden@uvm.edu
Abstract:
Members of the transient receptor potential (TRP) channel superfamily are present in vascular smooth muscle cells and play important roles in the regulation of vascular contractility. The TRPC3 and TRPC6 channels are activated by stimulation of several excitatory receptors in vascular smooth muscle cells. Activation of these channels leads to myocyte depolarization, which stimulates Ca2+ entry via voltage-dependent Ca2+ channels (VDCC), leading to vasoconstriction. The TRPV4 channels in arterial myocytes are activated by epoxyeicosatrienoic acids, and activation of the channels enhances Ca2+ spark and transient Ca2+-sensitive K+ channel activity, thereby hyperpolarizing and relaxing vascular smooth muscle cells. The TRPC6 and TRPM4 channels are activated by mechanical stimulation of cerebral artery myocytes. Subsequent depolarization and activation of VDCC Ca2+ entry is directly linked to the development of myogenic tone in vitro and to autoregulation of cerebral blood flow in vivo. These findings imply a fundamental importance of TRP channels in the regulation of vascular smooth muscle tone and suggest that TRP channels could be important targets for drug therapy under conditions in which vascular contractility is disturbed (e.g. hypertension, stroke, vasospasm).
Insights
Transient receptor potential (TRP) channels regulate vascular contractility. Different TRP channels cause vasoconstriction or vasodilation, highlighting their importance in blood flow regulation and potential as drug targets.
Area of Science:
- Physiology
- Molecular Biology
- Pharmacology
Background:
- Transient receptor potential (TRP) channels are key regulators of vascular smooth muscle cell function.
- These channels influence vascular contractility through mechanisms involving ion flux and membrane potential.
- Dysregulation of vascular contractility is implicated in various cardiovascular diseases.
Purpose of the Study:
- To elucidate the diverse roles of TRP channels in vascular smooth muscle.
- To understand how specific TRP channels (TRPC3, TRPC6, TRPV4, TRPM4) mediate vascular responses.
- To explore the therapeutic potential of targeting TRP channels for vascular disorders.
Main Methods:
- Investigated TRP channel activity in vascular smooth muscle cells.
- Examined the effects of receptor stimulation and mechanical stress on TRP channel function.
- Assessed the impact of TRP channel activation on myocyte depolarization, Ca2+ influx, and K+ channel activity.
Main Results:
- TRPC3 and TRPC6 activation by receptors leads to depolarization, Ca2+ entry via voltage-dependent Ca2+ channels (VDCC), and vasoconstriction.
- TRPV4 channels, activated by epoxyeicosatrienoic acids, enhance Ca2+ sparks and K+ channel activity, causing hyperpolarization and relaxation.
- TRPC6 and TRPM4 channels activated by mechanical stimuli contribute to myogenic tone and cerebral blood flow autoregulation.
Conclusions:
- TRP channels are fundamentally important in regulating vascular smooth muscle tone.
- Specific TRP channels mediate opposing effects on vascular contractility, influencing both constriction and relaxation.
- TRP channels represent promising therapeutic targets for conditions involving disturbed vascular contractility, such as hypertension and stroke.
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