Role of tyrosine kinase in erythrocyte lysate-induced contraction in rabbit cerebral arteries.

@article{Kim1998RoleOT,
  title={Role of tyrosine kinase in erythrocyte lysate-induced contraction in rabbit cerebral arteries.},
  author={C J Kim and K. W. Kim and J. W. Park and J. C. Lee and J. H. Zhang},
  journal={Journal of neurosurgery},
  year={1998},
  volume={89 2},
  pages={
          289-96
        }
}
OBJECT This study was undertaken to explore whether erythrocyte lysate, a proposed cause of vasospasm, produces vasoconstriction by activation of tyrosine kinase in rabbit cerebral arteries. METHODS Isometric tension was used to monitor contractions in rabbit basilar arteries induced by erythrocyte lysate, 5-hydroxytryptamine (5-HT), or KCl in the absence or presence of tyrosine kinase inhibitors. Erythrocyte lysate, 5-HT, or KCl produced concentration-dependent contractions in rabbit basilar… 
Mechanism of endothelin-1-induced contraction in rabbit basilar artery.
TLDR
It is demonstrated that MAPK may be involved in ET-1-induced contraction in rabbit basilar artery, which is downstream of PTK, Src, and Janus tyrosine kinase pathways but may not be downstream of phosphatidylinositol-3 Kinase pathways.
Mitogen-activated protein kinase plays an important role in hemolysate-induced contraction in rabbit basilar artery.
TLDR
Hemolysate produced contraction of rabbit basilar artery possibly by activation of MAPK, and pre-incubation of arteries with MAPK kinase inhibitor PD-98059 markedly reduced the contraction induced by hemolysates.
Role of protein tyrosine phosphorylation in erythrocyte lysate-induced intracellular free calcium concentration elevation in cerebral smooth-muscle cells.
TLDR
This is the first report to show that tyrosine phosphorylation may be involved in erythrocyte lysate-induced signal transduction and [Ca++]i responses in cerebral smooth-muscle cells.
Role of tyrosine kinase in fibroblast compaction and cerebral vasospasm.
TLDR
It is concluded that hemolysate activates tyrosine kinase that may lead to acceleration of fibroblast compaction that may contribute to cerebral vasospasm.
Attenuation of pressure‐induced myogenic contraction and tyrosine phosphorylation by fasudil, a cerebral vasodilator, in rat cerebral artery
TLDR
The present results suggest the inhibition by fasudil of pressure‐induced tyrosine phosphorylation and pp60src activation, and the wide spectrum of inhibitory actions of fasUDil may contribute to the effective attenuation of the pressure‐ induced contraction in the cerebral artery.
Relaxant Effect of U0126 in Hemolysate-, Oxyhemoglobin-, and Bloody Cerebrospinal Fluid–Induced Contraction in Rabbit Basilar Artery
TLDR
A role of MAPK in the contraction of rabbit basilar arteries by hemolysate, oxyhemoglobin, and bloody CSF is demonstrated, suggesting that U0126, a novel MAPK inhibitor, may be useful in the treatment of cerebral vasospasm.
Role of mitogen-activated protein kinase in the contractions of rabbit basilar artery induced by hemolysate, oxyhemoglobin, and bloody CSF.
TLDR
Mitogen-activated protein kinase (MAPK), a tyrosine kinase substrate, was activated by oxyhemoglobin (OxyHb) and hemolysate and contributed to cerebral arterial contraction and MAPK inhibitor PD98059 reduced the contraction of a rabbit basilar artery by hemolySate and endothelin-1.
Hemolysate induces tyrosine phosphorylation and collagen-lattice compaction in cultured fibroblasts.
TLDR
It is concluded that hemolysate activates tyrosine kinase that leads to the increase of fibroblast compaction, which may contribute to cerebral vasospasm.
Low [Mg2+]o induces contraction of cerebral arteries: roles of tyrosine and mitogen-activated protein kinases
TLDR
Activation of several cellular signaling pathways, such as protein tyrosine kinases (including the Src family and MAPK, appears to play important roles in low extracellular magnesium ion concentration-induced contractions and the elevation of Ca(2+)](i) in smooth muscle cells from canine basilar arteries.
Chronological Changes of the Contractile Mechanism in Prolonged Vasospasm after Subarachnoid Hemorrhage: From Protein Kinase C to Protein Tyrosine Kinase
TLDR
Results indicate that stiffness of the arterial wall increased and that the contractile property of the artery shifted from active myogenic tone to nonmyogenic tone, from PKC to PTK, with prolonged vasospasm.
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References

SHOWING 1-10 OF 36 REFERENCES
Role of Tyrosine Kinases in Norepinephrine‐Induced Contraction of Vascular Smooth Muscle
TLDR
The data indicate that genistein- and tyrphostin-sensitive tyrosine kinases participate in NE-induced contraction of rat aortic smooth muscle, and the enzymes appear to have a greater role in mediating the responses linked to the release of intracellular calcium.
Tyrosine kinase inhibitors suppress agonist-induced contraction in smooth muscle.
TLDR
The results suggest the novel hypothesis that tyrosine kinases participate in regulation of signal transduction that is associated with receptor-mediated contraction of smooth muscle.
Distinct signal transduction pathways for angiotensin-II in guinea pig gastric smooth muscle: differential blockade by indomethacin and tyrosine kinase inhibitors.
In guinea pig gastric longitudinal (LM) and circular (CM) muscle strips, angiotensin-II (Ang-II) caused a concentration-dependent contraction that required extracellular calcium and that could not be
Tyrosine phosphorylation and [Ca2+]i elevation induced by hemolysate in bovine endothelial cells: implications for cerebral vasospasm.
TLDR
Ca2+ and phosphotyrosine mediated cell signalling induced by hemolysate in endothelial cells may be activated by a single component but represent distinct targets for possible control of the cerebral vasospasm response.
Intracellular mechanisms involved in the responses of cerebrovascular smooth-muscle cells to hemoglobin.
TLDR
It is likely that activation of phospholipase C is a critical step in the development of vasospasm, but the transient nature of the response to inositol triphosphate suggests that the sustained contraction may arise from other phospholIPase C-dependent mechanisms.
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