Mechanism of Endothelin-1–Induced Contraction in Rabbit Basilar Artery

Zubkov, Alexander Y.; Rollins, K. Shadon; Parent, Andrew D.; Zhang, Junyi

doi:10.1161/01.str.31.2.526

Cited by 87 publications

(61 citation statements)

References 39 publications

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“…p42 / p44 MAPK may play a role in vascular smooth muscle contraction (11). Moreover, p42 / p44 MAPK may be an important regulator for rabbit basilar artery contraction (12). In contrast, p42 / p44 MAPK is † These authors contributed equally to this work.…”

Section: +mentioning

confidence: 99%

p38 Mitogen-Activated Protein Kinase Regulates Vasoconstriction in Spontaneously Hypertensive Rats

Kwon

Fang

et al. 2004

J Pharmacol Sci

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Abstract. We investigated whether p42 / p44 mitogen-activated protein kinase (MAPK) and / or p38 MAPK participates in the regulation of vascular smooth muscle contraction by endothelin-1 (ET-1) in Wistar-Kyoto rat (WKY) and spontaneously hypertensive rat (SHR). ET-1 (10 nM) induced a sustained contraction in WKY and SHR aortas. PD98059 (100 m M), an inhibitor of p42/ p44 MAPK kinase, partially attenuated the ET-1-induced contraction in WKY and SHR. However, SB203580 (10 m M), an inhibitor of p38 MAPK, relaxed the ET-1-induced contraction to the resting levels in SHR, but not in WKY. ET-1 (10 nM) increased phosphorylation of both p42 / p44 MAPK and p38 MAPK in WKY and SHR. However, in SHR, p38 MAPK phosphorylation in response to ET-1 stimulation was increased more than in WKY. PD98059 (100 m M) and SB203580 (10 m M) abolished the phosphorylation of p42 / p44 MAPK and p38 MAPK in response to ET-1 stimulation in WKY and SHR, respectively. On the other hand, SB203580 (10 mM) did not affect myosin light chain (MLC) phosphorylation in response to ET-1 (10 nM) stimulation in WKY and SHR. From these results, it is concluded that p42 / p44 MAPK and/ or p38 MAPK partially regulates the ET-1-induced vasoconstriction in WKY. However, p38 MAPK, rather than p42 / p44 MAPK, activation plays an important role for the maintenance of ET-1-induced vasoconstriction in SHR through a MLC phosphorylationindependent pathway.

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Section: +mentioning

confidence: 99%

p38 Mitogen-Activated Protein Kinase Regulates Vasoconstriction in Spontaneously Hypertensive Rats

Kwon

Fang

et al. 2004

J Pharmacol Sci

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“…Since class IB PI3-kinase ␥ regulates Ras-MAP kinase pathway and PI3-kinase inhibitor can attenuate ET-1-induced contraction and ET-1-induced MAP kinase activity, 12 class IB PI3-kinase ␥ may be involved in early vasospasm (which was not studied in the present study) by regulating Ras-MAP kinase. Thus, the time course of PI3-kinase activation during cerebral vasospasm, especially in the early stage, requires further investigation.…”

Section: Pi3-kinase and Vasospasmmentioning

confidence: 83%

“…37 PI3-kinase inhibitor also reduces angiotensin AT 1A receptor-stimulated and G␤␥ complexes-stimulated L-type Ca 2ϩ channel current in venous myocytes. 38 PI3-kinase inhibitors attenuate smooth muscle contraction induced by many G protein-coupled receptor agonists 12,14,16 and growth factors. 16 It is reported that PI3-kinase may act either downstream 39,40 or upstream from Ras protein in the signal transduction pathways.…”

Section: Pi3-kinase and Vasospasmmentioning

confidence: 99%

“…9,10 PI3-kinase can be activated by growth factors and by many G protein-coupled receptor agonists in smooth muscle cells. 11 Several investigators reported previously that PI3-kinase inhibitors attenuated the smooth muscle contraction induced by endothelin-1 (ET-1), 12 ATP, 13 5-hydroxytryptamine, 14 hydrogen peroxide, 15 thrombin, and epidermal growth factor. 16 To evaluate the role of PI3-kinase in the pathogenesis of delayed vasospasm, we applied 2 PI3-kinase inhibitors, wortmannin 17 and LY294002, 18 in an established canine doublehemorrhage model of SAH.…”

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confidence: 99%

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Phosphatidylinositol 3–Kinase Inhibitor Failed to Reduce Cerebral Vasospasm in Dog Model of Experimental Subarachnoid Hemorrhage

Kimura

Sasaki

Meguro

et al. 2002

Stroke

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Background and Purpose-Phosphatidylinositol 3-kinase (PI3-kinase) is involved in smooth muscle contraction induced by growth factors and/or G protein-coupled receptor agonists. To evaluate the role of PI3-kinase in the pathogenesis of delayed vasospasm, we applied 2 PI3-kinase inhibitors to an established canine double-hemorrhage model of experimental subarachnoid hemorrhage. Methods-Twenty-four dogs underwent double blood injections via the cisterna magna on days 0 and 2. The dogs were killed on day 7. Dogs were treated with either vehicle (dimethyl sulfoxide), wortmannin, or LY294002 once per day on day 2 through day 6. Angiography was performed before blood injection and before the dogs were killed. The basilar arteries were collected for morphology, Western blot analysis, and PI3-kinase activity. Results-The residual diameter of the basilar arteries in the dimethyl sulfoxide treatment group, which was compared with day 0 angiogram, decreased markedly on day 7 (the percentage of the residual diameter was 47.8Ϯ0.8%). Wortmannin and LY294002 did not significantly change residual diameter on day 7. Both PI3-kinase inhibitors abolished PI3-kinase activity compared with the vehicle treatment group. However, both PI3-kinase inhibitors failed to significantly attenuate PI3-kinase protein expression (Western blot) (PϾ0.05, ANOVA). Conclusions-Delayed

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“…The contribution of endothelin-1 to produce pathological changes of cerebral arteries after subarachnoid haemorrhage has been well studied (Asano et al 1990;Suzuki et al 1990;Caner et al 1996;Lampl et al 1997;Suzuki et al 2000;Yakubu et al 2000;Zubkov et al 2000), however, the details regarding its participation remain to be clarified. Previous studies (Dallaire et al 1992;Stanimirovic et al 1994;Nie & Olsson 1996;Dehouck et al 1997;Hernández et al 2000) have already noted and tried to examine the role of endothelin-1 in disrupting bloodbrain barrier permeability, but convincing evidence on the underlying mechanism has not been offered.…”

mentioning

confidence: 99%

Highly Enhanced Permeability of Blood‐Brain Barrier Induced by Repeated Administration of Endothelin‐1 in Dogs and Rats

Narushima¹,

Kita

Kubo³

et al. 2003

Pharmacology & Toxicology

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Abstract:The effects of intracisternal administration of endothelin-1 on blood-brain barrier permeability were examined in dogs and rats. Single doses of endothelin-1 elevated blood-brain barrier permeability about two times compared with control groups in both species. However, repeated dosing with endothelin-1 at a 24 hr intervals caused a highly enhanced disruption of blood-brain barrier permeability in dogs, but not in rats, whereas the repeated administration with a 48 hr interval markedly increased the blood-brain barrier permeability in both species of animals (dogs: 923%, rats: more than 661%). Moreover, this abnormally enhanced permeability of blood-brain barrier in dogs was completely blocked by pretreatment with the endothelin ET-A receptor selective antagonist, S-0139, administered prior to either the first or second dosing with endothelin-1. From these results, we conclude that a repeated attack of endothelin-1 from the adventitial site of brain blood vessels produces a severe disruption of blood-brain barrier permeability through an endothelin ET-A receptor-mediated process.

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Mechanism of Endothelin-1–Induced Contraction in Rabbit Basilar Artery

Cited by 87 publications

References 39 publications

p38 Mitogen-Activated Protein Kinase Regulates Vasoconstriction in Spontaneously Hypertensive Rats

p38 Mitogen-Activated Protein Kinase Regulates Vasoconstriction in Spontaneously Hypertensive Rats

Phosphatidylinositol 3–Kinase Inhibitor Failed to Reduce Cerebral Vasospasm in Dog Model of Experimental Subarachnoid Hemorrhage

Highly Enhanced Permeability of Blood‐Brain Barrier Induced by Repeated Administration of Endothelin‐1 in Dogs and Rats

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