Invited Symposium: Stroke/Cerebral Vasospasm |
Introduction Recently, several studies have suggested that intracellular second messenger systems, such as activation of phospholipase C (PLC), which generates inositol 1,4,5-triphosphate (IP3) and diacyglycerol (DAG), are involved in cerebral arterial contraction.7)8) We have previously reported that hemolysate-induced Ca2+ mobilization may be mediated through G protein-coupled P2u purinoceptors that activate phospholipase C.13) Protein tyrosine kinases have been suggested as another signal transduction mechanism to play an important role in the regulation of vascular smooth muscle tone.14)15) Receptor activation by agonists such as 5-HT, norepinephrine, angiotensin II, vasopressin and endothelin, not only activate PLC to generate IP3 and DAG, which activates protein kinase C (PKC), but also phosphorylates intermediate protein tyrosine kinases which regulate intracellular Ca2+ and smooth muscle contractility.14)15) We have shown previously that protein tyrosine kinase phosphorylation is triggered by hemolysate in cultured bovine endothelial cells as a cell signal to promote Ca2+ entry.16)
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Iwabuchi, S MD; Zhang, J MD PhD.; Aoki, K MD.; Marton, L PhD.; Kimura, H MD.; Samejima, H MD; (1998). Tyrosine Kinase In Cerebral Vasospasm. Presented at INABIS '98 - 5th Internet World Congress on Biomedical Sciences at McMaster University, Canada, Dec 7-16th. Invited Symposium. Available at URL http://www.mcmaster.ca/inabis98/zhang/iwabuchi0452/index.html | |||||||||||
© 1998 Author(s) Hold Copyright |