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Biomedical subjects

T Katsuragi

Publications and source records attributed to T Katsuragi.

At least 109 records · Page 6Linked to original sources
PubMed1981

Facilitation by clonidine of purine release induced by high KCl from the rabbit pulmonary artery.

1 The effect of clonidine on the 3H-purine release evoked by KCl or (-)-adrenaline was assessed in the superfused helical strip of the rabbit pulmonary artery pretreated with [3H]-adenosine. 2 Clonidine (3 x 10(-5) M to 10(-4) M) significantly enhanced the 3H-purine efflux evoked by 50 mM KCl but not by 3 x 10(-6) M) (-)-adrenaline. 3 This facilitatory effect of clonidine on the KCl-induced purine release was unaltered by phentolamine 3 x 10(-6) M. It was absent in arterial segments denervated with 6-hydroxydopamine 30 microgram/ml. 4 A sustained contractile response was evoked by clonidine 3 x 10(-5) M without an increase in the 3H-purine efflux. This was significantly reduced by phentolamine 3 x 10(-6) M, but not by yohimbine 10(-5) M or by denervation with 6-hydroxydopamine. 5 The uptake of [3H]-adenosine into the segments was not inhibited by clonidine 3 x 10(-5) M. 6 It is suggested that the facilitation by clonidine of the KCl-induced purine release is due to prevention of presynaptic autoinhibition of purine release from adrenergic nerves, by an antiadenosine action of the drug.

Adenosine↗
PubMed1980

Purine release from vascular adrenergic nerves by high potassium and a calcium ionophore, A-23187.

The effect of high KCl and a Ca++-ionophore, A-23187, on 3H-purine efflux from [3H]adenosine-labeled pulmonary artery and thoracic aortic media of the rabbit was assessed. High KCl (30, 50 and 70 mM) and A-23187 (5 microM) markedly enhanced the efflux from the adrenergically innervated pulmonary artery. The KCl-induced increase of 3H-efflux was greatly diminished by removal of Ca++ from the medium and pretreatment with 6-hydroxydopamine (30 micrograms/ml) and cold storage (4 days), but not by treatment with reserpine and phentolamine. In contrast, the 3H-efflux induced by l-epinephrine was not affected by cold storage or 6-hydroxydopamine but was inhibited by phentolamine. 3H-purine efflux by A-23187 was also significantly reduced by Ca++ removal or cold storage. In the nerve-free aortic medial preparation, the efflux inducing effects of both KCl and A-23187 were very limited. The remaining effect of KCl in this tissue was not Ca++-dependent. From these results the efflux of 3H-purines induced by the high KCl or Ca++-ionophore appears to originate mainly from the amine-containing vesicles in adrenergic nerve terminals, probably through the Ca++-dependent exocytosis. This supports the view that the release of ATP and norepinephrine are coupled in adrenergic neurotransmission.

Adrenergic Fibers↗
PubMed1979

Methysergide induces selective potentiation in cholinergic contractions of the guinea-pig vas deferens by facilitating acetylcholine release.

Methysergide (3 x 10(-6) M) enhanced the contractile responses of the isolated stripped vas deferens of guinea-pig to acetylchline(ACh) and arecoline, but not those to noradrenaline, tyramine and bradykinin. Methysergide (3 x 10(-5) M) suppressed the contraction elicited by noradrenaline or histamine. The methysergide-induced potentiation of the response to ACh was prevented by pre-addition of hemicholinium but not by tetrodotoxin or morphine. The augmentation of the response to ACh by physostigmine was unaffected by hemicholinium. The phasic contraction of the tissue elicited by 30 mM KCl was also enhanced by methysergide, and this enhancement was prevented by the pre-addition of atropine (1.4 x 10(-7) M). In the depolarized vas deferens after exposure to 30 mM KCl, methysergide occasionally induced a sustained tonic contraction which was inhibited by atropine. These findings suggest that methysergide facilitates a release of ACh by acting on the cholinergic nerve terminals and selectively potentiates the cholinergic response.

Acetylcholine↗
PubMed1979

Cholinergic potentiation by ouabain in the contraction of guinea-pig vas deferens through pre- and post-synaptic mechanism.

In the guinea-pig vas deferens, the contractions induced by pilocarpine and arecoline, unlike ACh, were markedly reduced by treatment with procaine (10(-6) g/ml) or hemicholinium (5 x 10(-4) g/ml). These reductions by hemicholinium were completely recovered after exposure to choline. The contractile responses to these three agonists were eliminated by atropine (3 x 10(-8) g/ml) but enhanced by neostigmine (3 x 10(-8) g/ml), though these were not affected at all by tetrodotoxin (3 x 10(-8) g/ml) or hexamethonium (10(-5) g/ml). The contractile responses to ACh, pilocarpine and arecoline were potentiated by ouabain (10(-6) g/ml). These potentiations were more marked in pilocarpine and arecoline than those in ACh. The potentiation in response to arecoline was maximal after incubation with ouabain for 5 min but that to ACh for 45 min. The results suggest that pilocarpine and arecoline act as ACh-releaser in this tissue and that the ouabain-induced cholinergic potentiation may be attributable to a dual mechanism, facilitation of ACh release at presynaptic site and alteration of the membrane excitability at postsynaptic site.

Animals↗
PubMed1978

Neuronal norepinephrine as mediator for ouabain-induced smooth muscle contraction.

With some latency, ouabain (10(-6)--10(-5) M) induced a long-lasting contractile response of the isolated vas deferens of the guinea-pig. The ouabain-induced contraction was potentiated by pretreatment with tropolone, whereas it was prevented by pretreatment with cocaine, bretylium, reserpine or phentolamine. The response was unaffected byatropine, methysergide and tetrodotoxin. Ouabain, perfused into the isolated tissue, enhanced dose-dependently the release of norepinephrine into the medium. However, this enhancement of norepinephrine release was prevented by reserpine or by removal of Ca from the medium. These findings support the hypothesis that the ouabain-induced contraction of vas deferens might be due to norepinephrine released from the adrenergic nerve ending granules through a Ca2+-dependent process.

Animals↗
PubMed1978

Vitamin B6 biosynthesis and nucleoside effect in the resting cell system of Flavobacterium sp. 238-7.

As one of the attempts to find clues on precursors or intermediates of the vitamin B6 biosynthetic pathway, the resting cell system of Flavobacterium sp. 238-7, a bacterium producing a high amount of the vitamin, was employed. Among various compounds tested as an additive to the reaction mixture, L-glutamate and nucleoside derivatives increased the formation of vitamin B6, respectively. The possible mechanism of the participation of these compounds in vitamin B6 biosynthesis is discussed. The identification of vitamin B6 formed in the reaction mixture was done using column chromatography.

Amino Acids↗
PubMed1978

Ouabain-induced potentiation of Ca2+-contraction in the depolarized vas deferens of guinea-pig.

The effect of ouabain (10(-5) M) on the Ca2+-evoked phasic contraction was examined in various depolarized vas deferens of the guinea-pig. Ouabain-induced potentiation of the contraction occurred in muscle depolarized with 40 mM K+, but not in muscle depolarized with 0 mM or 137 mM K+. Furthermore, this potentiating effect of ouabain was investigated in the presence of Mn2+ and Mg2+, each of which has an inhibitory effect on Ca2+-contraction. It was strongly inhibited by Mn2+, but unaffected by Mg2+. From these findings it is suggested that ouabain facilitates Ca2+-entry, which is accompanied by the spike generation.

Animals↗