ArticleBritish journal of pharmacology2006
Depletion of intracellular Ca2+ stores enhances flow-induced vascular dilatation in rat small mesenteric artery.
Article in British journal of pharmacology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 39 citations in OpenAlex.
- Irisin Regulates Cardiac Responses to Exercise in Health and Diseases: a Narrative Review.Journal of cardiovascular translational research · 2023Review
- High Salt Upregulates CaThe Journal of pharmacology and experimental therapeutics · 2022Article
- Protein kinase N2 mediates flow-induced endothelial NOS activation and vascular tone regulation.The Journal of clinical investigation · 2021Article
- Acetylcholine released by endothelial cells facilitates flow-mediated dilatation.The Journal of physiology · 2016Article
- Endothelial cation channel PIEZO1 controls blood pressure by mediating flow-induced ATP release.The Journal of clinical investigation · 2016Article
- Essential Role of Smooth Muscle STIM1 in Hypertension and Cardiovascular Dysfunction.Arteriosclerosis, thrombosis, and vascular biology · 2016Article
- Increasing TRPV4 expression restores flow-induced dilation impaired in mesenteric arteries with aging.Scientific reports · 2016Article
- P2Y₂ and Gq/G₁₁ control blood pressure by mediating endothelial mechanotransduction.The Journal of clinical investigation · 2015Article
- Vascular TRP channels: performing under pressure and going with the flow.Physiology (Bethesda, Md.) · 2014Review
- Ageing alters perivascular nerve function of mouse mesenteric arteries in vivo.The Journal of physiology · 2013Article
- Apigenin, a plant-derived flavone, activates transient receptor potential vanilloid 4 cation channel.British journal of pharmacology · 2012Article
- Depletion of intracellular Ca2+ stores stimulates the translocation of vanilloid transient receptor potential 4-c1 heteromeric channels to the plasma membrane.Arteriosclerosis, thrombosis, and vascular biology · 2010Article
- Blood ammonia levels in liver cirrhosis: a clue for the presence of portosystemic collateral veins.BMC gastroenterology · 2009Article
- Connexins in vascular physiology and pathology.Antioxidants & redox signaling · 2009Review
- Flow-induced enhancement of vasoconstriction and blockade of endothelium-derived hyperpolarizing factor (EDHF) by ascorbate in the rat mesentery.British journal of pharmacology · 2008Article
- Spreading dilatation to luminal perfusion of ATP and UTP in rat isolated small mesenteric arteries.The Journal of physiology · 2007Article
- Elevated pressure selectively blunts flow-evoked vasodilatation in rat mesenteric small arteries.British journal of pharmacology · 2007Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
The effect of depleting intracellular Ca2+ stores on flow-induced vascular dilatation and the mechanism responsible for the vasodilatation were examined in rat isolated small mesenteric arteries. The arteries were pressurized to 50 mmHg and preconstricted with phenylephrine. Intraluminal flow reversed the effect of phenylephrine, resulting in vasodilatation. Flow dilatation consisted of an initial transient peak followed by a sustained plateau phase. The magnitude of dilatation was markedly reduced by removing Ca2+ from the intraluminal flow medium. Depletion of intracellular Ca2+ stores with either cyclopiazonic acid (CPA, 2 microM) or 1,4-dihydroxy-2,5-di-tert-butylbenzene (BHQ, 10 microM) significantly augmented the magnitude of flow dilatation. Flow-induced endothelial cell Ca2+ influx was also markedly enhanced in arteries pretreated with CPA or BHQ.Flow-induced dilatation was insensitive to Nw-nitro-L-arginine methyl ester (100 microM) plus indomethacin (3 microM) or to oxyhemoglobin (3 microM), but was markedly reduced by 30 mM extracellular K+ or 2 mM tetrabutylammonium (TBA), suggesting an involvement of EDHF. Catalase at 1200 U ml-1 abolished the flow-induced dilatation, while the application of exogenous H2O2 (90-220 microM) induced relaxation in phenylephrine-preconstricted arteries. Relaxation to exogenous H2O2 was blocked in the presence of 30 mM extracellular K+, and H2O2 (90 microM) hyperpolarized the smooth muscle cells, indicating that H2O2 can act as an EDHF. In conclusion, flow-induced dilatation in rat mesenteric arteries can be markedly enhanced by prior depletion of intracellular Ca2+ stores. Furthermore, these data are consistent with a role for H2O2 as the vasodilator involved.
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