Reactive Oxygen Species Mediate the Suppression of Arterial Smooth Muscle T-type Ca2+ Channels by Angiotensin II

Scientific Reports
Ahmed M HashadDonald G Welsh

Abstract

Vascular T-type Ca2+ channels (CaV3.1 and CaV3.2) play a key role in arterial tone development. This study investigated whether this conductance is a regulatory target of angiotensin II (Ang II), a vasoactive peptide that circulates and which is locally produced within the arterial wall. Patch clamp electrophysiology performed on rat cerebral arterial smooth muscle cells reveals that Ang II (100 nM) inhibited T-type currents through AT1 receptor activation. Blocking protein kinase C failed to eliminate channel suppression, a finding consistent with unique signaling proteins enabling this response. In this regard, inhibiting NADPH oxidase (Nox) with apocynin or ML171 (Nox1 selective) abolished channel suppression highlighting a role for reactive oxygen species (ROS). In the presence of Ni2+ (50 µM), Ang II failed to modulate the residual T-type current, an observation consistent with this peptide targeting CaV3.2. Selective channel suppression by Ang II impaired the ability of CaV3.2 to alter spontaneous transient outward currents or vessel diameter. Proximity ligation assay confirmed Nox1 colocalization with CaV3.2. In closing, Ang II targets CaV3.2 channels via a signaling pathway involving Nox1 and the generation of ROS. This...Continue Reading

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Citations

Oct 9, 2018·Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism·Monica M Santisteban, Costantino Iadecola
Mar 19, 2019·Wiley Interdisciplinary Reviews. Systems Biology and Medicine·Matteo OttoliniSwapnil K Sonkusare
Sep 14, 2018·Journal of Smooth Muscle Research = Nihon Heikatsukin Gakkai Kikanshi·Shahnawaz Ahmad WaniSeemi Farhat Basir

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Methods Mentioned

BETA
confocal microscopy
proximity ligation assay
proximity ligation
Assay

Software Mentioned

Clampfit

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