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Biomedical subjects

H Ohshika

Publications and source records attributed to H Ohshika.

97 records · Page 6Linked to original sources
PubMed1983

Increase in potassium release from rat parotid tissue repeatedly exposed to isoproterenol.

The effect of repeated exposure to isoproterenol (ISO) in parotid tissue was investigated with regards to potassium release in response to a successive challenge of alpha- and beta-adrenergic agonists. An increase in potassium release by epinephrine was potentiated in the parotid tissue from rats repeatedly administered ISO (3 mg/kg, three times daily for 3 days). On the other hand, a decrease in the release by ISO disappeared in ISO-pretreated glands. Cycloheximide and actinomycin D, administered with ISO, completely blocked the ISO-induced development of the enhanced response to epinephrine, but not that of the reduced response to ISO. After in vitro pretreatment with ISO, the potassium release induced by a successive dose of ISO was higher than the basal release of the electrolyte. The same treatment showed a tendency to increase the response to norepinephrine. The increased release induced by a challenge dose of ISO disappeared in the tissue from cycloheximide-treated rats. The ISO-induced increase of potassium release which was caused by ISO-pretreatment in vitro was inhibited by prazosin, but not by yohimbin and propranolol. These results suggest the possibility that the alpha-adrenergic response in parotid tissue might be potentiated by exposure to ISO.

Animals↗
PubMed1982

Potentiation of isoproterenol-induced salivation by labetalol.

The authors previously reported that low doses of labetalol potentiated isoproterenol (ISO)-induced salivation in mice. The present study was carried out to ascertain the potentiating effect of labetalol in in vitro experiments using rat parotid tissue slices and their isolated cells. ISO-induced amylase release was enhanced by low concentrations of labetalol (less than 10(-6) M), while it was inhibited by high doses (more than 10(-5) M). This potentiating effect of labetalol did not occur in the Ca-free medium used for incubation or in experiments using the dispersed parotid cells or the parotid tissues which were obtained from 6-hydroxy-dopamine- or reserpine-treated rats. The effect of ISO on cyclic AMP accumulation in parotid tissue was completely blocked by the addition of labetalol in concentrations which were sufficient to increase the ISO-induced amylase release. Labetalol also inhibited the ISO-induced reduction of potassium release in parotid tissue. From these results, it is concluded that increases in the secretion of amylase and potassium from salivary glands due to the stimulation of glandular alpha-adrenoceptors by endogenous norepinephrine may play an important role in the potentiating effect of labetalol on ISO-induced salivation in mice.

Amylases↗
PubMed1981

Stimulating effect of alpha-adrenoceptor agonists on isoproterenol-induced amylase release in rat parotid tissue.

Isoproterenol (ISO)-induced amylase release from rat parotid slices was increased by the addition of methoxamine to either a normal or a calcium (Ca)-free medium. The potentiating effect of methoxamine was completely blocked by the addition of phentolamine, irrespective of whether the slices were incubated in the normal or the Ca-free medium; and the effect also disappeared after prolonged preincubation (60 min) of the slices in the Ca-free medium. Both verapamil and procaine reduced methoxamine-induced amylase release, but only verapamil blocked the stimulating effect of methoxamine in the normal medium. ISO-induced accumulation of cyclic AMP in the slices was unaffected by methoxamine or phenylephrine. The results suggest a possibility that the potentiating effect of methoxamine on ISO-induced amylase release may be independent of the presence of extracellular Ca and the increased accumulation of cyclic AMP in the tissue is unnecessary.

Adrenergic alpha-Agonists↗
PubMed1981

Relationship of carbon tetrachloride-induced alterations of ligandin and Z protein to sulfobromophthalein transport in rat liver.

The relationship of the BSP retaining capacity of organic anion binding protein in the liver to the transport of BSP from plasma to bile was examined in CCl4-treated rats. These proteins were separated into ligandin and Z protein by Sephadex G-75 gel chromatography. The BSP retaining capacity of these proteins was significantly decreased by CCl4 administration (2.5 ml/kg, p.o.). At 3 hours after CCl4, this decreased capacity was caused mainly by the decrease in their binding affinity, at 24 hours after CCl4, however, it was accompanied by decreases in both their binding affinity and protein amounts. At 3 hours, the hepatic uptake of BSP evaluated by determination of plasma BSP concentration, the initial disappearance rate (K1), and the hepatic dye content did not differ from those in the controls, and biliary excretion of BSP was unchanged. At 24 hours, hepatic uptake and biliary excretion of BSP as well as bile flow were significantly decreased. From these results, it is suggested that the alteration in the retaining capacity of ligandin and Z protein would not be a determinant factor in the transfer of BSP from plasma to bile.

Animals↗