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Biomedical subjects

F Hata

Publications and source records attributed to F Hata.

At least 127 records · Page 7Linked to original sources
PubMed1986

Autonomic nervous function determined by changes of periflux blood flow in the aged.

The periflux blood flow (PBF) in fingers was determined by a periflux laser Doppler flowmeter (PLDF). The patterns of PBF responses to standing and Valsalva's maneuver were analyzed. The PBF responses in both loading tests were well correlated with the results of the conventional autonomic function test. It was, therefore, considered that our method would be useful for assessment of autonomic function. We practically investigated PBF responses in the two loading tests in three groups: young age group (10-39 years), middle age group (40-69 years) and old age group (70-89 years). The old age group showed significant decreases in both sympathetic and parasympathetic functions. It was indicated that this non-surgical and simple autonomic function test will be useful particularly in the elderly.

Adolescent↗
PubMed1986

Dopamine-induced amylase secretion from rat parotid salivary gland in vitro: an effect mediated via noradrenergic and cholinergic nerves.

The effect of dopamine on amylase secretion by rat parotid tissue was examined in vitro. Dopamine induced marked amylase secretion from the tissue in a dose-dependent manner. Its EC50 value was about 4 microM and the maximal response was obtained at a concentration of 100 microM. The dopamine-induced secretion was inhibited by the dopamine-antagonists haloperidol, (+)-butaclamol and spiroperidol. Atropine reduced the dopamine-induced secretion significantly, and physostigmine enhanced the secretion. Parasympathectomy of the gland resulted in a significant decrease in the dopamine-induced secretion, but did not reduce the secretion induced by dopamine with atropine. Dopamine-induced ACh release from parasympathetic nerve terminals in the tissue was studied in tissue preparations that had been loaded with [3H]-choline. Dopamine elicited Ca2+-sensitive tritium release, and dopamine antagonists or parasympathectomy prevented this release. Sympathectomy or reserpine treatment of rats resulted in significant decrease in the dopamine-induced secretion, but increase in noradrenaline (NA)- or isoprenaline-induced secretion. Dopamine-induced NA release was studied by preloading the parotid tissue with [3H]-NA. Dopamine induced Ca2+-sensitive tritium release, and dopamine antagonists or sympathectomy prevented the release. Several lines of circumstantial evidence strongly suggested that dopamine has a specific site for action in the parotid tissue that is independent of NA receptors. In sympathectomized or reserpine-treated glands, atropine completely inhibited the dopamine-induced amylase secretion, suggesting that dopamine did not have a direct effect on postsynapses. These findings indicate that dopamine induces amylase secretion in two indirect ways mediated through ACh and NA released from parasympathetic and sympathetic nerve terminals, respectively.

Amylases↗
PubMed1985

Prevention of supersensitivity-like phenomena in rat vas deferens by colchicine.

Rat vas deferens has been shown to become supersensitive to alpha-adrenergic agonists on brief treatment with epinephrine (Epi-treatment). Epi-treatment increased the contractile response and the number of alpha-adrenoceptors in the tissue. The application of colchicine (2.5 mM) during Epi-treatment prevented the supersensitivity-like phenomena and increase in number of alpha-adrenoceptors. Vinblastine (10 microM) also counteracted the effect of Epi-treatment but cytochalasin B (100 microM) and strychnine (2.5 mM) did not. It is suggested that the supersensitivity-like phenomena induced in rat vas deferens by Epi-treatment were due to a change in microtubular components of the membrane.

Animals↗
PubMed1985

Forskolin induces supersensitivity of the amylase secretory response of rat parotid tissue.

The stimulatory effect of forskolin on amylase secretion was studied by pretreating rat parotid tissue with forskolin for 10 min, incubating it in medium without forskolin for 10 min, and then treating it with forskolin again. Pretreatment with 10 microM forskolin for 10 min resulted in increased amylase secretion and enhanced accumulation of cyclic AMP in the tissue during the second incubation with forskolin. In the presence of colchicine or vinblastine, the enhancement in cyclic AMP accumulation during the second incubation with forskolin was prevented, but the increased amylase secretion remained unchanged. The increased amylase secretion was counteracted only in the presence of concanavalin A. On the other hand, increased amylase secretion induced by isoproterenol (IPR) pretreatment was counteracted by colchicine, vinblastine, concanavalin A or strychnine. These data suggest that the total amount of cyclic AMP in the tissue does not have any essential role in the supersensitivity of the amylase secretory response, and that the supersensitivity induced by forskolin differs from that induced by IPR.

Amylases↗
PubMed1984

Effect of strychnine on the contractile response of rat vas deferens.

Strychnine at concentrations of 0.1 approximately 1.0 microM induced supersensitivity of rat vas deferens to alpha-agonists but not to other stimulants. Strychnine-treatment resulted in an increase in the number of alpha-adrenoceptors, determined by measuring the binding of [3H]prazosin. Glycine did not have any significant effect on the contracture and did not antagonize the action of strychnine. Thus, specific supersensitivity of alpha-adrenergic system was induced by treatment with low concentrations of strychnine.

Animals↗
PubMed1983

beta-Adrenoceptor alterations coupled with secretory response in rat parotid tissue.

Simultaneous studies on the secretory response of amylase and the neurotransmitter receptors of rat parotid gland, after brief treatment with agonists, showed selective alteration in beta-adrenoceptors with specific change in amylase secretion, suggesting a regulatory role of the receptors in the secretory response. The beta-adrenergic agonist (+/-)-isoprenaline (IPR) stimulated amylase secretion from rat parotid tissues much more than did the same concentration of an alpha-adrenergic or cholinergic agonist. The stimulatory effects of IPR were studied by pre-treating rat parotid tissues with IPR for 10 min and then incubating the tissue in fresh medium for 10 min. Pre-treatment with 10 microM-IPR for 10 min resulted in increased amylase secretion during further incubation with IPR and also in a lower EC50 value of amylase secretion for IPR. This treatment also resulted in selective changes in the number and affinity of beta-adrenoceptors, assessed by measuring binding of [3H]dihydroalprenolol (DHA): the maximal binding sites increased from 286/357 f-mole to mg protein and the IC50 value (the concentration for 50% inhibition of specific [3H]DHA binding) of beta-agonists, not antagonists, decreased significantly. An increase in the period of pre-treatment with IPR to 30 min resulted in a decrease in the maximal binding sites of beta-adrenoceptors and a decrease in amylase secretion during further incubation with IPR. Experiments with other agonists showed that supersensitivity of the secretory response was induced specifically by beta-agonists. Binding studies with [3H]WB-4101 and [3H]quinuclidinyl benzilate showed that alpha-adrenoceptors and muscarinic ACh receptors in rat parotid did not change under the conditions tested. The alteration in beta-adrenoceptors was parallel with a change in amylase secretion after IPR pre-treatment, but not with a change in cyclic AMP content.

Acetylcholine↗
PubMed1982

Characteristics of [3H]E-643-binding to alpha adrenoceptors.

Radiolabeled E-643, a newly developed antihypertensive compound, bound specifically to a preparation obtained from rat brain with a maximum of 85 f moles of binding sites per mg protein and a dissociation constant of 0.59 nM. Prazosin markedly inhibited the binding. While yohimbine and clonidine were only weak inhibitors. Other characteristics of the binding of [3H]E-643 to the brain and its specific binding to preparations of peripheral rat organs were also studied. The present findings suggest that [3H]E-643 is useful for labeling alpha 1-adrenoceptors.

Adrenergic alpha-Agonists↗