1990 Fiscal Year Final Research Report Summary
Functional Interaction Between Adrenergic Receptor Subtypes In the intracellular Signal Transduction.
| Project/Area Number |
01570110
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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 |
General pharmacology
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| Research Institution | Sapporo Medical College |
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Principal Investigator |
OHSHIKA Hideyo Sapporo Medical College The Medical Department Professor, 医学部, 教授 (50045358)
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| Co-Investigator(Kenkyū-buntansha) |
KIMURA Hisakazu Sapporo Medical College The Medical Department Instructor, 医学部, 助手 (20204985)
TAKEMURA Haruo Sapporo Medical College The Medical Department Instructor, 医学部, 助手 (20106462)
HATTA Shinichi Sapporo Medical College The Medical Department Instructor, 医学部, 助手 (60094223)
MIYAMOTO Atsushi Sapporo Medical College The Medical Department Assistant Prof., 医学部, 講師 (50166196)
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| Project Period (FY) |
1989 – 1990
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| Keywords | Adrenergic Receptors / Aging / G Proteins / Cultured Myocytes / Intracellular Sodium Ion / Inositol Phosphates |
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| Research Abstract |
A possible interaction of receptor function between alpha- and beta-adrenergic receptor subtypes was studied about binding sites for specific radioligands, G proteins and second messengers in the intracellular signal transduction system. (1) Mechanism of functional compensation for a decrease of receptor number in the aged rats : Although alpha-1 adrenergic receptor decreased both in heart and cerebral cortex, the generation of inositol phosphates induced by alpha-1 adrenergic stimulation was low in heart and high in cerebral cortex. It was suggested that the change of membrane fluidity was partly responsible for the change of cellular alpha-1 adrenergic responses. The number of beta adrenergic receptors decreased both in heart and parotid gland. The states of activity of adenylate cyclase were resulted from the impairment of Gs function in hearts and the impairment of Gi function in parotid cells. (2) The modification of receptor function by the changes of intracellular distribution o
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f ions : An increased [Na^+] _i in rat parotid acinar cells caused the amylase release via the increase of [Ca^<2+>] _i . However, amylase release induced by beta-agonistOr dibutyryl cAMP was suppressed by the increased [Na^+] _i . Since the elevation of [Na^+] _i did not change adenylate cyclase activity, it may be responsible for the regulation of intracellular cAMP function. (3) Analysis of adrenergic receptor function of primary cultured neonatal rat cardiac myocytes during development : The increase of heart rate by beta-adrenergic stimulation developed in parallel with the maturation of cytoskeleton structure. The heart rate was increased by high concentration of phenylephrine, but decreased by its low concentration. Alpha-1 antagonist enhanced the stimulating effect of the agonist, but it caused a diminution of the suppressing effect of the agonist. Treatment with beta-agonist for 24 hours caused diminished response to high concentration of alpha-1 agonist and a strongly enhanced response to its lower concentration. Less
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