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F Hata

Publications and source records attributed to F Hata.

At least 145 records · Page 8Linked to original sources
PubMed1981

Role of alpha-adrenergic receptors in denervation supersensitivity of rat vas deferens.

Contractile responses of rat vas deferens were studied with particular attention directed to the role of receptors and neuronal control. Marked contraction of the vas deferens was observed with alpha-adrenergic agonists, depending on their concentrations. This tissue had a low sensitivity to ACh. Four days after denervation, this tissue showed a supersensitivity to alpha-adrenergic agonists and a high K+ concentration, but not to ACh. The increase in sensitivity to alpha-agonists resulted in an enhancement of the maximal response and a shift of the concentration response curve to lower concentrations of these reagents. Alterations were seen in the alpha-adrenergic receptors in the rat vas deferens, assayed by measuring the binding of [3H]WB4101. The maximal binding sites decreased significantly to 86 from 142 fmoles per mg protein. The affinity of the receptors for alpha-agonist, determined by measuring the ability of agonists to displace bound [3H] WB4101, increased significantly, while the affinity to alpha-antagonists remained unchanged. Studies on [3H]QNB binding indicated no significant change in muscarinic ACh receptors after denervation. Thus, supersensitivity of the alpha-adrenergic mechanism mediated by a specific change in affinity of alpha-receptors occurs after denervation of rat vas deferens. These changes in sensitivity and in receptors are discussed in relation to the characteristics and roles of alpha-receptors in the rat vas deferens.

Acetylcholine↗
PubMed1980

Increase in response and number of alpha-adrenoceptors of rat vas deferens on brief pretreatment with an alpha-agonist.

The contractile response of rat vas deferens to epinephrine (E) was enhanced by preincubation with E. After pretreatment with E, there was no significant change in the ED50 of E but there was a significant increase in the maximum response (39%). There was no change in the cholinergic response after the pretreatment. alpha-Adrenoceptors in control and E-treated tissues were assessed by measuring [3H]WB-4101 binding. Treatment with E resulted in a 27% increase in the number of alpha-adrenoceptors, but no change in muscarinic acetylcholine receptors measured with [3H]quinuclidinyl benzilate. These results are discussed in relation to the response of alpha-adrenoceptors to the agonist.

Adrenergic alpha-Agonists↗
PubMed1980

Specific changes in the cholinergic system in guinea-pig vas deferens after denervation.

A small rapid phase (1st phase) was distinguished from a concomitant phase (2nd phase) in contraction of guinea-pig vas deferens. The vas deferens 4 days after denervtion exhibited supersensitivity to stimulants. The supersensitivity in the 2nd phase of contraction was nonspecific, but that in the 1st phase was specific to muscarinic cholinergic agonists. The increase in sensitivity resulted in a shift of the dose-response curve to lower concentrations without significant change in the maximal response. Muscarinic cholinergic receptors in the vas deferens, determined by measuring binding of [3H]quinuclidinyl benzilate, changed after denervation. The maximal binding sites increased from 115 to 165 fmol/mg of protein with no significant change in the dissociation constant. The affinity of the receptor for agonist also did not change significantly. Studies on [3H]WB4101 binding indicated no significant change in alpha adrenergic receptors after denervation. Thus, specific supersensitivity of the cholinergic mechanism mediated by muscarinic acetylcholine receptors occurred after denervation of guinea-pig vas deferens. This increased sensitivity is discussed in relation to the amount of receptor.

Acetylcholine↗
PubMed1979

Distribution of PNMT and epinephrine in the medulla oblongata of normotensive and spontaneous hypertensive rats.

The distribution of the Epinephrine forming enzyme (PNMT) activity and Epinephrine (E) levels was investigated in the medulla oblongata of spontaneous hypertensive rats (SH-rats) and in two normotensive strains, namely Wistar Kyoto rats (WK-rats) and Wistar rats. The PNMT activity increases progressively from the caudal to rostral parts in the C1 and C2 regions of the medulla oblongata. The enzyme activity and the E levels are in all parts of the C1 and C2 regions higher in Wistar rats than in WK-rats. The PNMT activity in all parts of the C2 region (with the exception of the caudal region), and in the middle part of the C1 region is higher in SH-rats than in WK-rats. The E levels in the SH-rats are higher than in WK-rats in the mediocaudal parts of the C2 and C1 regions.

Animals↗
PubMed1978

Bromocriptine, lergotrile: the antiparkinsonian efficacy and the interaction with monoaminergic receptors.

The antiparkinsonian activity of bromocriptine and of lergotrile was investigated in monkeys with surgically induced tremor and in parkinsonian patients. Both drugs effectively relieve tremor in experimental monkeys and induce less pronounced abnormal involuntary movements than L-dopa or piribedil. Both drugs were shown to be of therapeutic value in a group of patients with advanced Parkinson's disease who were no longer responsive to levodopa combined with carbidopa. Adverse effects were similar to those observed with levodopa and carbidopa, except that in individual patients abnormal involuntary movements and diurnal oscillations in performance ("on-off" effect) were decreased, while mental changes were increased. The interactions of bromocriptine and of lergotrile with dopamine and alpha-adrenergic receptors were investigated. Both drugs have mixed agonist-antagonist activities with respect to the dopamine receptors; lergotrile has a higher affinity for the agonist site while bromocriptine has a higher affinity for the antagonist site of the receptors. Both drugs effectively displace the binding of the alpha-adrenergic antagonist WB-4101 to cerebral cortex membranes. The mechanisms underlying the antiparkinsonian efficacies of these two drugs were discussed.

Animals↗
PubMed1978

Binding interactions of ergot alkaloids with monoaminergic receptors in the brain.

The interactions of ergot alkaloids and of other drugs with dopamine (DA) and alpha-adrenergic receptors were investigated. The tested ergot alkaloids inhibit synaptosomal tyrosine hydroxylase activity and reverse the apomorphine-elicited inhibition of synaptosomal tyrosine hydroxylase activity. Thus, ergot alkaloids interact as both agonists and antagonists with the presynaptic DA receptors. Ergot alkaloids also compete effectively for the binding of 3H-DA and 3H-haloperidol to bovine striatal membranes. These results show that these drugs are mixed agonist-antagonists with respect to the postsynaptic DA receptors. To determine the effects of ergot alkaloids and of neuroleptics on the alpha-adrenergic receptors in the CNS, we have measured their effects on the binding of 3H-dihydroergocryptine and 3H-WB-4101 to cerebral cortical membranes. The displacing potencies of the tested ergot alkaloids and of the neuroleptics indicated that they have a high affinity for the alpha-adrenoreceptors in the CNS. The mechanisms underlying the therapeutic efficacy of mixed agonist-antigonists of DA and alpha-adrenergic receptors in Parkinson's disease and in geriatric disorders were considered.

Animals↗
PubMed1978

Effects of synaptic plasma membranes on release of acetylcholine from synaptic vesicles.

The influences of synaptic plasma membranes on release of acetylcholine (ACh) from synaptic vesicles isolated from rat brain were examined. In the presence of ATP, Mg++ and Ca++ but absence of cytoplasm from the nerve endings, the synaptic plasma membranes did not increase ACh release indicating absence of a stimulating factor which is known to be present in the cytoplasm. In presence of ATP, Mg++, Ca++ and the cytoplasm, the synaptic plasma membranes inhibited ACh release from the synaptic vesicles in high K+ medium, though not in high Na+ medium. Binding of Ca++ by the synaptic plasma membranes was dependent on ATP, inhibited by Na+ and stimulated by K+. Thus, the synaptic plasma membranes may inhibit ACh release in high K+ medium due to reduction in the concentration of free Ca++.

Acetylcholine↗
PubMed1977

The interactions of bromocriptine and lergotrile with dopamine and alpha-adrenergic receptors.

Bromocriptine and lergotrile, which are clinically used as antiparkinsonian (AP) agents, compete for the binding of H3-dopamine, H3-apomorphine, and H3-haloperidol to striatal membrane sites. Lergotrile has a higher affinity for the H3-dopamine binding to bovine striatal membranes than bromocriptine. Lergotrile and bromocriptine are almost equipotent in competing for the binding of H3-apomorphine to rat striatal membranes, but bromocriptine is more potent in competing for the binding of H3-haloperidol than lergotrile. These results indicate that lergotrile and bromocriptine are mixed putative agonist-antagonist with respect to the postsynaptic dopamine receptors. Lergotrile and bromocriptine at higher concentrations inhibit synaptosomal tyrosine hydroxylase activity, and reverse the apomorphine elicited enzyme inhibition. Thus, these ergot alkaloids behave as mixed agonist-antagonist also with respect to the presynaptic dopamine receptors. Bromocriptine and lergotrile, as well as other tested DH-ergot alkaloids and neuroleptics, compete for the binding of the alpha-antagonist H3-WB-4101 to rat cerebral cortical membranes. The displacing potencies of the tested DH-ergot alkaloids and of the neuroleptics indicate that they have a high affinity for the alpha-adrenoreceptors in the CNS.

Acetonitriles↗
PubMed1976

Effects of Na+ and other monovalent cations on Ca-efflux from synaptosomes.

Effects of monovalent cations on Ca-efflux were examined in rat brain cortex slices, synaptosomes and synaptic plasma membranes. Effluxes of 45Ca from brain slices and synaptosomes were stimulated by Na+ in medium and the effects of Na+ on the 45Ca-effluxes disappeared at low temperature. Furthermore, we observed that Rb+ had more effect than Na+ on 45Ca-efflux from the synaptosomes, while Li+ had less effect. On the other hand, release of 45Ca from the synaptic plasma membranes which had been preincubated with ATP, MG++ and 45Ca was stimulated by Na+ and Li+. But Cs+ and Rb+ were less effective on the release. These results indicate occurrence of Na-dependent Ca-efflux at nerve endings. However, the assumption that ATP-dependent Ca-binding with synaptic plasma membranes may be a partial reaction of Ca-efflux was not supported by these experiments.

Animals↗