ArticleAmerican journal of physiology. Cell physiology2015
Angiotensin II stimulates internalization and degradation of arterial myocyte plasma membrane BK channels to induce vasoconstriction.
Article in American journal of physiology. Cell physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 45 citations in OpenAlex.
- Renin-Angiotensin Signaling and Vascular Function: Insights into Health and Disease.Acta physiologica (Oxford, England) · 2026Review
- Potassium channels in vascular smooth muscle cells.Physiological reviews · 2026Review
- Uncoupling of CaProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Vasodilators mobilize SK3 channels in endothelial cells to produce arterial relaxation.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Loss of IP3R-BKInternational journal of molecular sciences · 2023Article
- Perinatal Fat-Diets Increased Angiotensin II-Mediated CaNutrients · 2023Article
- Rab GTPases as Modulators of Vascular Function.Cells · 2022Review
- Angiotensin II-induced endothelial dysfunction: Impact of sex, genetic background, and rho kinase.Physiological reports · 2022Article
- Large-Conductance Calcium-Activated Potassium Channel Opener, NS1619, Protects Against Mesenteric Artery Remodeling Induced by Agonistic Autoantibodies Against the Angiotensin II Type 1 Receptor.Journal of the American Heart Association · 2022Article
- The Footprint of Kynurenine Pathway in Cardiovascular Diseases.International journal of tryptophan research : IJTR · 2022Review
- Pathogenesis-based preexposure prophylaxis associated with a low risk of SARS-CoV-2 infection in healthcare workers at a designated COVID-19 hospital: a pilot study.BMC infectious diseases · 2021Article
- Age-dependent decrease in TRPM4 channel expression but not trafficking alters urinary bladder smooth muscle contractility.Physiological reports · 2021Article
- Non-immune Prophylaxis Against COVID-19 by Targeting Tolerance for Angiotensin II-Triggered SARS-CoV-2 Pathogenesis.Frontiers in medicine · 2021Article
- Coronary Large Conductance CaFrontiers in physiology · 2021Review
- BK channel density is regulated by endoplasmic reticulum associated degradation and influenced by the SKN-1A/NRF1 transcription factor.PLoS genetics · 2020Article
- Targeting BKCNS drugs · 2020Review
- Calcium- and voltage-gated BK channels in vascular smooth muscle.Pflugers Archiv : European journal of physiology · 2018Review
- Impaired Trafficking of β1 Subunits Inhibits BK Channels in Cerebral Arteries of Hypertensive Rats.Hypertension (Dallas, Tex. : 1979) · 2018Article
- Chronic interval exercise training prevents BKJournal of applied physiology (Bethesda, Md. : 1985) · 2018Article
- Angiotensin II Promotes KHypertension (Dallas, Tex. : 1979) · 2018Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Arterial smooth muscle cells (myocytes) express large-conductance Ca(2+)-activated K(+) (BK) channel α and auxiliary β1 subunits that modulate arterial contractility. In arterial myocytes, β1 subunits are stored within highly mobile rab11A-positive recycling endosomes. In contrast, BKα subunits are primarily plasma membrane-localized. Trafficking pathways for BKα and whether physiological stimuli that regulate arterial contractility alter BKα localization in arterial myocytes are unclear. Here, using biotinylation, immunofluorescence resonance energy transfer (immunoFRET) microscopy, and RNAi-mediated knockdown, we demonstrate that rab4A-positive early endosomes traffic BKα to the plasma membrane in myocytes of resistance-size cerebral arteries. Angiotensin II (ANG II), a vasoconstrictor, reduced both surface and total BKα, an effect blocked by bisindolylmaleimide-II, concanavalin A, and dynasore, protein kinase C (PKC), internalization, and endocytosis inhibitors, respectively. In contrast, ANG II did not reduce BKα mRNA, and sodium nitroprusside, a nitric oxide donor, did not alter surface BKα protein over the same time course. MG132 and bafilomycin A, proteasomal and lysosomal inhibitors, respectively, also inhibited the ANG II-induced reduction in surface and total BKα, resulting in intracellular BKα accumulation. ANG II-mediated BK channel degradation reduced BK currents in isolated myocytes and functional responses to iberiotoxin, a BK channel blocker, and NS1619, a BK activator, in pressurized (60 mmHg) cerebral arteries. These data indicate that rab4A-positive early endosomes traffic BKα to the plasma membrane in arterial myocytes. We also show that ANG II stimulates PKC-dependent BKα internalization and degradation. These data describe a unique mechanism by which ANG II inhibits arterial myocyte BK currents, by reducing surface channel number, to induce vasoconstriction.
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