2014
DOI: 10.1161/strokeaha.114.005544
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ATP-Evoked Sustained Vasoconstrictions Mediated by Heteromeric P2X1/4 Receptors in Cerebral Arteries

Abstract: Background and Purpose-Current knowledge states that vasoconstrictor responses to ATP are mediated by rapidly desensitizing ligand-gated P2X1 receptors in vascular smooth muscle cells (VSMCs). However, ATP is implicated in contributing to pathological conditions involving sustained vasoconstrictor response such as cerebral vasospasm. The purpose of this study is to test the hypothesis that the stimulation of VSMC P2XR receptors (P2XRs) contributes to ATPevoked sustained vasoconstrictions in rat middle cerebral… Show more

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Cited by 15 publications
(8 citation statements)
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“…The effects of P2X 4 R blockade were negligible on renal hemodynamics in ANG II-infused rats in contrast to the effects of the P2X 1 R and P2X 7 R antagonists despite expression of these receptors on renal vessels. These data suggest that a conformational change of P2X 4 R induced by ANG II would impair the interaction with the antagonist (49) or the presence of heteromeric P2X 1 R/ 4 R, which would induce vasoconstriction (14). Nevertheless, in sham-operated rats the P2X 4 R antagonist induced renal vasoconstriction and reduced glomerular hemodynamics, results that were similar to those of the hypertensive group; this effect could be attributed to a blockade of NO release induced by P2X 4 R inhibition, or alterations in the tone of the smooth muscle cells mediated by these receptors.…”
Section: Glomerular Microcirculation Under P2x 4 Receptors Blockadementioning
confidence: 90%
“…The effects of P2X 4 R blockade were negligible on renal hemodynamics in ANG II-infused rats in contrast to the effects of the P2X 1 R and P2X 7 R antagonists despite expression of these receptors on renal vessels. These data suggest that a conformational change of P2X 4 R induced by ANG II would impair the interaction with the antagonist (49) or the presence of heteromeric P2X 1 R/ 4 R, which would induce vasoconstriction (14). Nevertheless, in sham-operated rats the P2X 4 R antagonist induced renal vasoconstriction and reduced glomerular hemodynamics, results that were similar to those of the hypertensive group; this effect could be attributed to a blockade of NO release induced by P2X 4 R inhibition, or alterations in the tone of the smooth muscle cells mediated by these receptors.…”
Section: Glomerular Microcirculation Under P2x 4 Receptors Blockadementioning
confidence: 90%
“…The P2X1 receptor is the main post-junctional receptor for ATP in small resistance-sized arteries, though the expression of other vascular smooth muscle P2X receptors have been identified in different vascular beds [18]. The non-selective cation current passed during P2X1 opening in smooth muscle cells can stimulate vasoconstriction via several mechanisms.…”
Section: J O U R N a L P R E -P R O O Fmentioning
confidence: 99%
“…The non-selective cation current passed during P2X1 opening in smooth muscle cells can stimulate vasoconstriction via several mechanisms. These include direct elevation in intracellular Ca 2+ through inward movement of Ca 2+ through the channel itself, and membrane depolarisation caused by the non-selective cation current and subsequence opening of voltage-gated Ca 2+ channels [18,29]. Endothelial P2X1 has also been reported to stimulate vasodilation via Ca 2+activated K + channels in some blood vessels [20].…”
Section: J O U R N a L P R E -P R O O Fmentioning
confidence: 99%
“…Stimulation of sympathetic nerves releases norepinephrine and ATP in the smooth muscle layer of blood vessels; these two potent vasoconstrictors are upregulated in hypertension [117]. ATP exerts transient vasoconstriction mostly through activation of the P2X1R on vascular smooth muscle cells (VSMCs) [118,119], followed by a smaller yet sustained contraction via P2X4R activation [120]. Both P2X1R and P2X4R localized on VSMCs contribute to vasospasm occurring as a consequence of hemorrhagic stroke [120].…”
Section: Cardiovascular Risk Factors: Is the P2x4 Receptor Friend Or mentioning
confidence: 99%
“…In the late stage of atherosclerosis, erosion and plaque rupture occurs leading to endothelial cells damage and inability to prevent thrombotic events, thus prompting acute coronary and stroke events. Endothelial damage exposes not only the procoagulant and platelet-aggregating features of subendothelial matrix proteins [6] but also the vasoconstrictive P2X1R and P2X4R on VSMCs to surplus amounts of ATP derived from platelet aggregation and damaged cells [119,120]. Thus, one may hypothesize that the P2X4R exerts a protective role in blood vessels when the endothelium is functional, but its action is detrimental once blood vessels are severely damaged, such as in acute coronary and aortic syndromes, as well as in stroke.…”
Section: Cardiovascular Risk Factors: Is the P2x4 Receptor Friend Or mentioning
confidence: 99%