1994 Fiscal Year Final Research Report Summary
PHYSIOLOGICAL SIGNIFICANSE OF THE PATHWAY OF MONOVALENT CATIONS ON THE Ca STORES IN THE INTRACELLULAR SIGNAL TRANSDUCTION OF VASCULAR CELLS
| Project/Area Number |
05837017
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
血管生物学
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| Research Institution | KYUSHU UNIVERSITY |
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Principal Investigator |
YAMAMOTO Hiromichi KYUSHU UNIV.FACULTY OF MEDICINE RESEARCH ASSOCIATE, 医学部, 助手 (20166820)
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| Project Period (FY) |
1993 – 1994
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| Keywords | Vascular cells / Calcium ion / Monovalent ions / Signal transduction |
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| Research Abstract |
1.ATP-dependent ^<45>Ca^<2+> uptake into and efflux from intracellular Ca^<2+> stores were measured in saponin-skinned smooth muscle cells which were primary cultured from the rat aorta.
2.When 130 mM KC1 of the buffer solution was substituted for LiC1, Tris・HC1, NH4C1, choline chloride or sucrose, the efflux rate increased. However, it did not change in case of RbC1, CsC1 and NaC1. Valinomycin either inhibited or modified these changes. These results suggested that there exist potential-sensitive Ca^<2+> release channels on the membrane of the stores and that they were opened by the substitution of KC1 for impermeable monovalent cations.
3.When KC1 was substituted for choline chloride, Tris・HC1, LiC1, ^<45>Ca^<2+> uptake was inhibited remarkably. It was suggested that inhibitory effects of these cations on potassium efflux from the stores possibly suppressed Ca^<2+> uptake.
4.Effects of substitution on KC1 for vharious monovalent cations or sucrose on inositol tris phosphate-induced Ca^<2+> release (IICR) were examined in the presence and absence of 300 nM Ca^<2+>. From the magnitude of inhibition of IICR caused by the substitution of KC1, it was able to estimate changes in membrane potential and, hence, an order of relative permeability of monovalent cations.
5.Effects of substitution of KC1 for various monovalent cations or sucrose on Ca^<2+>-or caffieine-induced Ca^<2+> release (CICR) were examined. It was shown that the substitution of KC1 might have changed membrane potential to become negative inside the store and inhibited CICR.However, unlike IICR,it was also suggested that Ca^<2+> itself could give influence to cation-permeable channels.
6.In conclusion, it was suggested that Ca^<2+> uptake into and release from the intracellular stores in rat aortic smooth muscle cells were regulated by the movement of monovalent cations through the membrane of the stores.
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Research Products
(6 results)
