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Cited by 512

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Transient Receptor Potential Channels Regulate Myogenic Tone of Resistance Arteries

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Welsh, Donald G., Morielli, Anthony D., Nelson, Mark T., Brayden, Joseph E.·2002·Circulation Research

Abstract

Elevation of intravascular pressure causes depolarization and constriction (myogenic tone) of small arteries and arterioles, and this response is a key element in blood flow regulation. However, the nature of pressure-induced depolarization has remained elusive. In the present study, we provide evidence that a transient receptor potential channel (TRPC6) homologue has a major role in this depolarizing response to pressure. Antisense oligodeoxynucleotides to TRPC6 decreased TRPC6 protein expression and greatly attenuated arterial smooth muscle depolarization and constriction caused by elevated pressure in intact cerebral arteries. Suppressing the expression of this channel protein also reduced the current density of a major cation current in resistance artery smooth muscle cells. We propose that TRPC6 channels play an essential role in regulation of myogenic tone.

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Metadata

Authors
Welsh, D. G., Morielli, A. D., Nelson, M. T., & Brayden, J. E.
Venue
Circulation Research
Published
2002-02-22
Volume
90
Issue
3
Pages
248-250
ISSN
  • 0009-7330 (ISSN-L)
  • 1524-4571
OpenAlex
W2036082842
Cited by
512
References
0
FWCI
10.41
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Transient Receptor Potential Channels Regulate Myogenic Tone of Resistance Arteries. https://app.cochat.ai/papers/10.1161/hh0302.105662
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Welsh, D. G., Morielli, A. D., Nelson, M. T., & Brayden, J. E. (2002). Transient Receptor Potential Channels Regulate Myogenic Tone of Resistance Arteries. Circulation Research. https://doi.org/10.1161/hh0302.105662

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.