Rapid increase in inositol phosphate levels in norepinephrine-stimulated vascular smooth muscle
Autor: | E. F. Labelle, Hong Gu, R. J. Barsotti, H. Martin |
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Rok vydání: | 1991 |
Předmět: |
Tail
medicine.medical_specialty Vascular smooth muscle Physiology Inositol Phosphates Inositol 1 4 5-Trisphosphate Biology Muscle Smooth Vascular Norepinephrine (medication) chemistry.chemical_compound Norepinephrine Internal medicine medicine Animals Inositol Inositol phosphate Chromatography High Pressure Liquid chemistry.chemical_classification Inositol trisphosphate Cell Biology Arteries Rats Kinetics Endocrinology chemistry Second messenger system Catecholamine medicine.symptom medicine.drug Muscle contraction Muscle Contraction |
Zdroj: | The American journal of physiology. 261(1 Pt 1) |
ISSN: | 0002-9513 |
Popis: | We examined the correlation between agonist-stimulated increases in inositol phosphates and force development in vascular smooth muscle. Segments of rat tail artery were preincubated with [3H]inositol and treated with norepinephrine (10(-5) M) for 3-10 s. Tissue levels of inositol monophosphate (IP), inositol bisphosphate (IP2), and inositol trisphosphate (IP3) were measured. IP and IP2 increased significantly after 3 s of norepinephrine treatment. IP3 increased significantly after 5 s of norepinephrine treatment. Analysis of tissue extracts by high-pressure liquid chromatography demonstrated that the only isomer of IP3 present in any tissue extract was the 1,4,5-isomer [Ins(1,4,5)P3]. Contractile response to norepinephrine stimulation showed that the increase in inositol phosphates coincides well with the time course of force development. This is the first report demonstrating such an early increase in Ins(1,4,5)P3 in agonist-stimulated vascular smooth muscle. These results are consistent with the hypothetical role of Ins(1,4,5)P3 as a mediator linking agonist-receptor activation to increased intracellular calcium and force development in norepinephrine-stimulated vascular smooth muscle. |
Databáze: | OpenAIRE |
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