Evidence map›Paper›PMID 26069238›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2015

Genetic ablation of CaV3.2 channels enhances the arterial myogenic response by modulating the RyR-BKCa axis.

Osama F Harraz, Suzanne E Brett, Anil Zechariah, Monica Romero, Jose L Puglisi, Sean M Wilson, Donald G Welsh

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.7field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

35 citing papers in PubMed, 45 citations in OpenAlex.

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  12. Vascular calcium signalling and ageing.The Journal of physiology · 2021
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  15. Long-Term Hypoxia Negatively Influences CaFrontiers in physiology · 2021
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  17. Aging, calcium channel signaling and vascular tone.Mechanisms of ageing and development · 2020
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 2 countries.

Osama F HarrazFrom the Department of Physiology and Pharmacology, Hotchkiss Brain and Libin Cardiovascular Institutes, University of Calgary, Calgary, Alberta, Canada (O.F.H., S.E.B., A.Z., D.G.W.); Department of Pharmacology and Toxicology, Alexandria University, Alexandria, Egypt (O.F.H.); Department of Basic Sciences, Division of Pharmacology, Loma Linda University, CA (M.R., S.M.W.); Department of Pharmacology, University of California, Davis (J.L.P.); and Department of Physiology and Pharmacology, University of Western Ontario, London, Ontario, Canada (D.G.W.).
Suzanne E BrettFrom the Department of Physiology and Pharmacology, Hotchkiss Brain and Libin Cardiovascular Institutes, University of Calgary, Calgary, Alberta, Canada (O.F.H., S.E.B., A.Z., D.G.W.); Department of Pharmacology and Toxicology, Alexandria University, Alexandria, Egypt (O.F.H.); Department of Basic Sciences, Division of Pharmacology, Loma Linda University, CA (M.R., S.M.W.); Department of Pharmacology, University of California, Davis (J.L.P.); and Department of Physiology and Pharmacology, University of Western Ontario, London, Ontario, Canada (D.G.W.).
Anil ZechariahFrom the Department of Physiology and Pharmacology, Hotchkiss Brain and Libin Cardiovascular Institutes, University of Calgary, Calgary, Alberta, Canada (O.F.H., S.E.B., A.Z., D.G.W.); Department of Pharmacology and Toxicology, Alexandria University, Alexandria, Egypt (O.F.H.); Department of Basic Sciences, Division of Pharmacology, Loma Linda University, CA (M.R., S.M.W.); Department of Pharmacology, University of California, Davis (J.L.P.); and Department of Physiology and Pharmacology, University of Western Ontario, London, Ontario, Canada (D.G.W.).
Monica RomeroFrom the Department of Physiology and Pharmacology, Hotchkiss Brain and Libin Cardiovascular Institutes, University of Calgary, Calgary, Alberta, Canada (O.F.H., S.E.B., A.Z., D.G.W.); Department of Pharmacology and Toxicology, Alexandria University, Alexandria, Egypt (O.F.H.); Department of Basic Sciences, Division of Pharmacology, Loma Linda University, CA (M.R., S.M.W.); Department of Pharmacology, University of California, Davis (J.L.P.); and Department of Physiology and Pharmacology, University of Western Ontario, London, Ontario, Canada (D.G.W.).
Jose L PuglisiFrom the Department of Physiology and Pharmacology, Hotchkiss Brain and Libin Cardiovascular Institutes, University of Calgary, Calgary, Alberta, Canada (O.F.H., S.E.B., A.Z., D.G.W.); Department of Pharmacology and Toxicology, Alexandria University, Alexandria, Egypt (O.F.H.); Department of Basic Sciences, Division of Pharmacology, Loma Linda University, CA (M.R., S.M.W.); Department of Pharmacology, University of California, Davis (J.L.P.); and Department of Physiology and Pharmacology, University of Western Ontario, London, Ontario, Canada (D.G.W.).
Sean M WilsonFrom the Department of Physiology and Pharmacology, Hotchkiss Brain and Libin Cardiovascular Institutes, University of Calgary, Calgary, Alberta, Canada (O.F.H., S.E.B., A.Z., D.G.W.); Department of Pharmacology and Toxicology, Alexandria University, Alexandria, Egypt (O.F.H.); Department of Basic Sciences, Division of Pharmacology, Loma Linda University, CA (M.R., S.M.W.); Department of Pharmacology, University of California, Davis (J.L.P.); and Department of Physiology and Pharmacology, University of Western Ontario, London, Ontario, Canada (D.G.W.).
Donald G WelshFrom the Department of Physiology and Pharmacology, Hotchkiss Brain and Libin Cardiovascular Institutes, University of Calgary, Calgary, Alberta, Canada (O.F.H., S.E.B., A.Z., D.G.W.); Department of Pharmacology and Toxicology, Alexandria University, Alexandria, Egypt (O.F.H.); Department of Basic Sciences, Division of Pharmacology, Loma Linda University, CA (M.R., S.M.W.); Department of Pharmacology, University of California, Davis (J.L.P.); and Department of Physiology and Pharmacology, University of Western Ontario, London, Ontario, Canada (D.G.W.). dwelsh@ucalgary.ca.
Loma Linda University · USAlexandria University · EGUniversity of California, Davis · US

Funding

Intrauterine chronic hypoxia and ryanodine receptors in fetal pulmonary arteriesR03HD069746 · NICHD · LOMA LINDA UNIVERSITY · PI WILSON, SEAN M · 2012 to 2013
$145k
Canadian Institutes of Health Research MOP-69088NICHD NIH HHS HD069746NICHD NIH HHS R03 HD069746
6 · The paper itself

Abstract

objectiveIn resistance arteries, there is an emerging view that smooth muscle CaV3.2 channels restrain arterial constriction through a feedback response involving the large-conductance Ca(2+)-activated K(+) channel (BKCa). Here, we used wild-type and CaV3.2 knockout (CaV3.2(-/-)) mice to definitively test whether CaV3.2 moderates myogenic tone in mesenteric arteries via the CaV3.2-ryanodine receptor-BKCa axis and whether this regulatory mechanism influences blood pressure regulation. APPROACH AND

resultsUsing pressurized vessel myography, CaV3.2(-/-) mesenteric arteries displayed enhanced myogenic constriction to pressure but similar K(+)-induced vasoconstriction compared with wild-type C57BL/6 arteries. Electrophysiological and myography experiments subsequently confirmed the inability of micromolar Ni(2+), a CaV3.2 blocker, to either constrict arteries or suppress T-type currents in CaV3.2(-/-) smooth muscle cells. The frequency of BKCa-induced spontaneous transient outward K(+) currents dropped in wild-type but not in knockout arterial smooth muscle cells upon the pharmacological suppression of CaV3.2 channel. Line scan analysis performed on en face arteries loaded with Fluo-4 revealed the presence of Ca(2+) sparks in all arteries, with the subsequent application of Ni(2+) only affecting wild-type arteries. Although CaV3.2 channel moderated myogenic constriction of resistance arteries, the blood pressure measurements of CaV3.2(-/-) and wild-type animals were similar.

conclusionsOverall, our findings establish a negative feedback mechanism of the myogenic response in which CaV3.2 channel modulates downstream ryanodine receptor-BKCa to hyperpolarize and relax arteries.

Indexed as

VasoconstrictionVasodilationAnimalsArterial PressureCalcium Channel BlockersCalcium Channels, T-TypeCalcium SignalingFeedback, PhysiologicalFemaleLarge-Conductance Calcium-Activated Potassium Channel alpha SubunitsMaleMesenteric ArteriesMice, Inbred C57BLMice, KnockoutMuscle, Smooth, VascularMyocytes, Smooth MuscleBKCa protein, mouseCacna1h protein, mouseCalcium Channel BlockersCalcium Channels, T-TypeKcnma1 protein, mouseLarge-Conductance Calcium-Activated Potassium Channel alpha SubunitsRyanodine Receptor Calcium Release Channelarteriescalcium-activated potassium channelscalcium channelscalcium signalingryanodine receptorsT-type calcium channelsvascular smooth muscle

Identifiers

PMID26069238
PMCPMC5117108
OpenAlexW2099253123

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.