ArticleThe Journal of physiology2013
Endothelial alkalinisation inhibits gap junction communication and endothelium-derived hyperpolarisations in mouse mesenteric arteries.
Article in The Journal of physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
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- The conducted vasomotor response and the principles of electrical communication in resistance arteries.Physiological reviews · 2024Review
- The solution to bicarbonate.American journal of physiology. Heart and circulatory physiology · 2022Article
- Ion Channels, Transporters, and Sensors Interact with the Acidic Tumor Microenvironment to Modify Cancer Progression.Reviews of physiology, biochemistry and pharmacology · 2022Review
- Exacerbation of Epilepsy by Astrocyte Alkalization and Gap Junction Uncoupling.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
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- Acid-base regulation and sensing: Accelerators and brakes in metabolic regulation of cerebrovascular tone.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2018Review
- Murine breast cancer feed arteries are thin-walled with reduced αBreast cancer research : BCR · 2018Article
- Carbonic anhydrase inhibitors modify intracellular pH transients and contractions of rat middle cerebral arteries during COJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2018Article
- Piezo1 channels sense whole body physical activity to reset cardiovascular homeostasis and enhance performance.Nature communications · 2017Article
- Contribution of K(+) channels to endothelium-derived hypolarization-induced renal vasodilation in rats in vivo and in vitro.Pflugers Archiv : European journal of physiology · 2016Article
- Extracellular HCO3- is sensed by mouse cerebral arteries: Regulation of tone by receptor protein tyrosine phosphatase γ.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2016Article
- Perivascular tissue inhibits rho-kinase-dependent smooth muscle Ca(2+) sensitivity and endothelium-dependent H2 S signalling in rat coronary arteries.The Journal of physiology · 2015Article
- Endothelial control of vasodilation: integration of myoendothelial microdomain signalling and modulation by epoxyeicosatrienoic acids.Pflugers Archiv : European journal of physiology · 2014Review
- Regulation of cellular communication by signaling microdomains in the blood vessel wall.Pharmacological reviews · 2014Review
- Intracellular acidification alters myogenic responsiveness and vasomotion of mouse middle cerebral arteries.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2014Article
- Disturbed acid-base transport: an emerging cause of hypertension.Frontiers in physiology · 2013Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Abstract Gap junctions mediate intercellular signalling in arteries and contribute to endothelium-dependent vasorelaxation, conducted vascular responses and vasomotion. Considering its putative role in vascular dysfunction, mechanistic insights regarding the control of gap junction conductivity are required. Here, we investigated the consequences of endothelial alkalinisation for gap junction communication and endothelium-dependent vasorelaxation in resistance arteries. We studied mesenteric arteries from NMRI mice by myography, confocal fluorescence microscopy and electrophysiological techniques. Removing CO2/HCO3(-), reducing extracellular [Cl(-)] or adding 4,4-diisothiocyanatostilbene-2,2-disulphonic acid inhibited or reversed Cl(-)/HCO3(-) exchange, alkalinised the endothelium by 0.2-0.3 pH units and inhibited acetylcholine-induced vasorelaxation. NO-synthase-dependent vasorelaxation was unaffected by endothelial alkalinisation whereas vasorelaxation dependent on small- and intermediate-conductance Ca(2+)-activated K(+) channels was attenuated by ∼75%. The difference in vasorelaxation between arteries with normal and elevated endothelial intracellular pH (pHi) was abolished by the gap junction inhibitors 18β-glycyrrhetinic acid and carbenoxolone while other putative modulators of endothelium-derived hyperpolarisations - Ba(2+), ouabain, iberiotoxin, 8Br-cAMP and polyethylene glycol catalase - had no effect. In the absence of CO2/HCO3(-), addition of the Na(+)/H(+)-exchange inhibitor cariporide normalised endothelial pHi and restored vasorelaxation to acetylcholine. Endothelial hyperpolarisations and Ca(2+) responses to acetylcholine were unaffected by omission of CO2/HCO3(-). By contrast, dye transfer between endothelial cells and endothelium-derived hyperpolarisations of vascular smooth muscle cells stimulated by acetylcholine or the proteinase-activated receptor 2 agonist SLIGRL-amide were inhibited in the absence of CO2/HCO3(-). We conclude that intracellular alkalinisation of endothelial cells attenuates endothelium-derived hyperpolarisations in resistance arteries due to inhibition of gap junction communication. These findings highlight the role of pHi in modulating vascular function.
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