Vascular Dopamine-I Receptors

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著者

    • YASUNARI Kenichi
    • First Department of Internal Medicine, Osaka City University, Medical School
    • KOHNO Masakazu
    • First Department of Internal Medicine, Osaka City University, Medical School
    • YOKOKAWA Koji
    • First Department of Internal Medicine, Osaka City University, Medical School
    • HORIO Takeshi
    • First Department of Internal Medicine, Osaka City University, Medical School
    • KANO Hiroaki
    • First Department of Internal Medicine, Osaka City University, Medical School
    • TAKEDA Tadanao
    • First Department of Internal Medicine, Osaka City University, Medical School

抄録

The modulation of dopamine DA<sub>1</sub> receptors of cultured rat renal arterial smooth muscle cells by phorbol ester, glucocorticoid and sodium chloride was studied. The extent of [<sup>3</sup>H]Sch-23390 binding to phorbol ester-treated cell was increased without any change in the dissociation constant (<i>K</i><sub>d</sub>). At a concentration of 10nmol/l, the synthetic glucocorticoid dexamethasone increased maximum receptor binding (<i>B</i><sub>max</sub>) but had no effect on the <i>K</i><sub>d</sub>. 100mmol/l sodium chloride did not change <i>B</i><sub>max</sub>, but increased the <i>K</i><sub>d</sub> for DA<sub>1</sub> receptor. The production of cAMP in response to DA<sub>1</sub> receptor stimulation was enhanced without any change of the adenylate cyclase activity. The glucocorticoid effect on DA<sub>1</sub> of arterial smooth muscle cells became apparent after hours of incubation in the presence of the steroid and was significantly inhibited by cycloheximide (10μg/ml) and by the glucocorticoid receptor antagonist RU- 38486, indicating that the effect required protein synthesis through glucocorticoid receptors. Treatment of cells with 1μmol/l dexamethasone for 24h increased basal and DA<sub>1</sub>-stimulated adenylate cyclase activity. Basal adenylate cyclase was decreased by sodium chloride in a dose-dependent manner. These results suggest differential control of DA<sub>1</sub> receptors on vascular smooth muscle cells by protein kinase C, glucocorticoid or sodium chloride. (<i>Hypertens Res</i> 1995; 18 Suppl. I: S29-S33)

収録刊行物

  • Hypertension research : clinical and experimental : official journal of the Japanese Society of Hypertension

    Hypertension research : clinical and experimental : official journal of the Japanese Society of Hypertension 18, S29-S33, 1995-06-01

    The Japanese Society of Hypertension

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