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T Kashimoto

Publications and source records attributed to T Kashimoto.

At least 37 records · Page 2Linked to original sources
PubMed1995

Ginseng saponins reduce acetylcholine-evoked Na+ influx and catecholamine secretion in bovine adrenal chromaffin cells.

The effects of various ginseng saponins (ginsenosides Rb1, Rb2, Rb3, Rc, Rd, Re, Rf, Rg1, Rg2, Rh1, Ro and Rs1), which are isolated from the root of Panax ginseng, on the catecholamine secretion from bovine adrenal chromaffin cells stimulated by ACh were examined. Most of the ginsenosides (1-100 microM) had a tendency to reduce the ACh-evoked secretion of catecholamines. The order of inhibitory potency (at the concentration of 10 microM) was as follows: Rg2 > Rf > Re > Rh1 > Rb2, Rg1 > Rb1 > Rc > Rb3, Rd, Ro, Rs1. The inhibition of ginseoside Rg2 at 10 microM was 72%, but ginsenosides Rb3, Rd, Ro and Rs1 did not show the inhibitory effect. On the other hand, ginsenoside Rg2 (1-100 microM) did not at all affect the secretion induced by high K+ or veratridine, a potent specific activator of voltage-sensitive Na+ channels. Ginsenoside Rg2 (1-100 microM) also inhibited both ACh-induced Na+ and Ca++ influxes into the cells in a concentration-dependent manner. The concentration-response curves for ginsenoside Rg2 inhibition of Na+ influx, of Ca++ influx and of catecholamine secretion were quite similar. The inhibitory effect of ginsenoside Rg2 on the secretion was not overcome by increasing ACh or external Ca++ concentrations. These results strongly suggest that the ginseng saponins, especially ginsenoside Rg2, block the nicotinic ACh receptors or the receptor-operated Na+ channels (but not voltage-sensitive Na+ and Ca++ channels), inhibit Na+ influx through the channels and consequently reduce both Ca++ influx and catecholamine secretion in bovine adrenal chromaffin cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1995

Dimethylsulfoxide potentiates the suppressive effects of lidocaine on synaptic transmission in bullfrog sympathetic ganglion.

The effects of dimethylsulfoxide used as a solvent on the suppressive effects of lidocaine on synaptic transmission were examined in the bullfrog sympathetic ganglion. Compound action potentials (CAP) in response to orthodromic stimulation of the presynaptic nerve trunk were recorded extracellularly from the bullfrog sympathetic ganglion. Application of lidocaine dissolved in normal Ringer's solution significantly decreased the amplitude of CAP. This suppressive effect of lidocaine was markedly potentiated when lidocaine was dissolved in 0.1% DMSO solution. A similar potentiating effect of DMSO was observed on the suppressive action of lidocaine on acetylcholine (ACh)-induced depolarizing response recorded intracellularly from the sympathetic ganglion cell. On the other hand, 0.1% DMSO solution alone had no effect on synaptic transmission, resting membrane potential, resting membrane resistance or ACh receptor activity. The present findings suggest that DMSO as solvent should be used carefully because of its potentiating effect on drug actions. Since the effect of lidocaine is due to the suppression of nicotinic ACh receptor at the postsynaptic membrane, DMSO may allosterically act on the nicotinic ACh receptor causing an increase in efficacy of lidocaine.

Acetylcholine↗
PubMed1994

Effects of SK&F 96365, an inhibitor of receptor-mediated Ca2+ entry, on Ca2+ influx and catecholamine secretion in bovine adrenal chromaffin cells.

SK&F 96365 (1-[3-(4-methoxyphenyl)propoxyl]-1-(4-methoxyphenyl)ethyl-1H- imidazole HCl) (1-50 microM), an inhibitor of receptor-mediated Ca2+ entry, reduced both acetylcholine (ACh)- and 56 mM K+ (high K+)-induced 45Ca2+ influxes and catecholamine secretion in bovine adrenal chromaffin cells. However, SK&F 96365 at lower concentrations (1-3 microM) inhibited only ACh-induced 45Ca2+ influx and secretion but not their high K(+)-induction. In Na(+)-free medium, ACh-induced 45Ca2+ influx and secretion were also considerably decreased by SK&F 96365 at low concentrations (1-3 microM). These results suggest that in the chromaffin cells, not only voltage-sensitive calcium channels but also ACh receptor-operated calcium channels at least in part contribute to the influx of Ca2+ which triggers the catecholamine secretion from the cells when the cells are exposed by ACh.

Acetylcholine↗
PubMed1993

Involvement of phosphoinositide turnover in ouabain inotropism.

We examined whether ouabain activities phospholipases and reinforces contraction force of papillary muscles through resultant second messengers. 2-Nitro-4-carboxyphenyl-N,N-diphenylcarbamate (NCDC), the inhibitor of phospholipase C (PLC), abolished the ouabain inotropy in rabbit papillary muscles. Calphostin C, the specific inhibitor of protein kinase C (PKC), also depressed the ouabain inotropy. 12-O-Tetradecanoylphorbor-13-acetate (TPA), the specific activator of PKC, enhanced the beat-to-beat phasic contractility at low concentrations. Radioenzymatic assay revealed that ouabain treatment doubled diacylglycerol (DG) content in excised papillary muscles. We concluded that ouabain activates PLC, and the resultant second messenger, DG, augments the cardiac contraction force through activation of PKC.

Animals↗
PubMed1993

Cisplatin, an antineoplastic drug, inhibits catecholamine secretion from bovine adrenal chromaffin cells.

Long-term pretreatment (12-120 h) of cultured bovine adrenal chromaffin cells with cis-diamminedichloroplatinum (cisplatin, Pt(NH3)2Cl2) (33 microM), an antineoplastic drug, resulted in a decrease in the secretion of catecholamines from the cells stimulated by acetylcholine. Acetylcholine-induced 45Ca2+ influx into the cells was also reduced in the cells pretreated with cisplatin for 48 h. The concentration-response curves (3-66 microM) for cisplatin inhibition of the secretion and 45Ca2+ influx were quite similar. Pretreatment of cells with 33 microM Pt4+ or carboplatin, an analog of cisplatin, for 48 h also led to a decrease in acetylcholine-evoked secretion, but not with 33 microM Pt2+ or other metals (Au+, Au3+, Ni2+, Os3+, Pd2+, Ir3+, and Ir4+) that have properties similar to Pt4+. These results strongly suggest that in bovine adrenal chromaffin cells, cisplatin (3-66 microM) inhibits catecholamine secretion by the suppression of the Ca2+ influx into the cells evoked by acetylcholine and that the inhibitory effect of cisplatin is attributable to the tetravalent platinum ion in its molecule.

Acetylcholine↗
PubMed1993

Effects of antiallergic drugs on catecholamine secretion from bovine adrenal chromaffin cells.

The effects of the antiallergic drugs, oxatomide, ibudilast, and tranilast on catecholamine secretion from bovine adrenal chromaffin cells stimulated by acetylcholine were examined. Both oxatomide (2-100 microM) and ibudilast (10-100 microM) resulted in the inhibition of the secretion of catecholamines from the cells in a concentration-dependent manner, whereas tranilast (100 nM-100 microM) did not. Oxatomide and ibudilast also reduced the acetylcholine-induced 45Ca2+ influx into the cells. The concentration-response curves for oxatomide and ibudilast inhibiting 45Ca2+ influx were quite similar to those for drugs inhibiting the secretion. Oxatomide similarly reduced both high K(+)-induced 45Ca2+ influx and secretion. However, the oxatomide inhibition of acetylcholine-induced secretion was not overcome by increasing the concentrations of acetylcholine or Ca2+. Oxatomide also inhibited histamine-induced secretion and the inhibition was almost overcome by increasing histamine concentration. These results indicate that oxatomide and ibudilast inhibit catecholamine secretion from bovine adrenal chromaffin cells stimulated by acetylcholine. The inhibition is due to the suppression of Ca2+ influx into the cells through voltage-dependent Ca2+ channels. The results further suggest that oxatomide competitively antagonizes histamine receptors and inhibits the secretion stimulated by histamine.

Acetylcholine↗
PubMed1992

Effects of gentamicin on catecholamine levels in the striatum, hypothalamus, adrenal gland and vas deferens.

The effects of gentamicin, an aminoglycoside antibiotic, on changes in the catecholamine levels in the rat striatum, hypothalamus, adrenal medulla and vas deferens were studied. When rats were i.v. injected with gentamicin (1.0 mg/kg), the catecholamine content of all tissues increased 2-4 h after injection. The increases in catecholamine levels induced by gentamicin were about 1.4- to 2.3-fold those induced by saline. The effect of gentamicin was observed at 0.1 or 0.5 mg/kg, and was maximal at 2.0 mg/kg. The activity of tyrosine hydroxylase, a rate-limiting enzyme in catecholamine biosynthesis, was markedly increased in all four tissues of rats treated with gentamicin (1.0 mg/kg, 4 h). However, direct addition of gentamicin to the tyrosine hydroxylase assay medium did not affect tyrosine hydroxylase activity. These data indicate that gentamicin administration to rats increases the catecholamine content of both central and peripheral catecholamine-containing tissues. The results also suggest that the effect of gentamicin is due to an indirect activation of tyrosine hydroxylase.

Adrenal Medulla↗
PubMed1991

[Study on the limitation for detecting anaerobic threshold by respiratory frequency].

It has been reported that respiratory frequency (F) serves to determine anaerobic threshold (AT). The purpose of this study was to investigate whether the method detecting AT by using F is influenced by the subject's condition such as the existence of sport experiences. Ten healthy adults volunteered to perform progressive cycle ergometer exercise with workloads increased by 30-W (female:20-W) every 2 min at 60 rpm. VO2 at AT were determined by four different methods, which detect the point of 1)nonlinear increase in VE, VCO2, and increase in VE/VO2 without increasing in VE/VCO2 (AT-v), 2) nonlinear increase in F (visual estimation: AT-VF), 3) inflection in F by multisegment linear regression (AT-CF), 4) inflection with omitting above RC point as with 3) (AT-CF2). The mean VO2 at AT-VF (40.8 +/- 9.2 ml/kg/min) and AT-CF (42.7 +/- 9.9 ml/kg/min) was significantly higher compared with AT-V (28.2 +/- 10.4 ml/kg/min) and not RC (42.3 +/- 10.0 ml/kg/min). It would be possible that AT-VF and AT-CF indicated RC, but not AT. There were no significant differences between AT-CF2 (28.2 +/- 10.9 ml/kg/min) and AT-V, and a highly positive correlation (r = 0.79, p less than 0.05) was observed between them. It was recognized that F reached a plateau at AT in four of the subjects. The error between AT-V and AT-CF2 was observed individual variations and the error between them within 5% was observed in only one subject. These results suggest that F is inadequate as an indicator of the AT, because F may be influenced by entrainment of breathing and pedalling frequency.

Adult↗
PubMed1991

Trichosporin-B-III, an alpha-aminoisobutyric acid-containing peptide, causes Ca(2+)-dependent catecholamine secretion from adrenal medullary chromaffin cells.

We examined the effect of trichosporin-B-III, an alpha-aminoisobutyric acid-containing antibiotic peptide consisting of 19 amino acid residues and a phenylalaninol, on catecholamine secretion from cultured bovine adrenal chromaffin cells. Incubation of the cells with trichosporin-B-III (3-20 microM) caused an increase in the secretion of catecholamines. The secretion induced by trichosporin-B-III at low concentrations (3 and 5 microM) was completely dependent on external Ca2+, whereas that induced by higher concentrations (10 and 20 microM) was partly independent of Ca2+. Trichosporin-B-III at low concentration (5 microM) did not increase the release of lactate dehydrogenase, a marker enzyme of cytoplasm, from the cells. In contrast, the peptide at higher concentration (10 microM) increased the release of the enzyme. Trichosporin-B-III also caused both 45Ca2+ influx into the cells and an increase in the intracellular free Ca2+ concentration. The increases in catecholamine secretion and 45Ca2+ influx behaved similarly in relation to trichosporin-B-III concentration (3-10 microM). The time courses of the increases in secretion, 45Ca2+ influx, and intracellular free Ca2+ concentration induced by trichosporin-B-III were also quite similar. Trichosporin-B-III-induced (at 5 microM) secretion was not affected by the elimination of Na+ from the incubation medium or by the addition of tetrodotoxin, a blocker of highly selective voltage-dependent Na+ channels, or hexamethonium, a blocker of nicotinic acetylcholine receptors. On the other hand, both diltiazem (2-200 microM) and nicardipine (1-200 microM), blockers of voltage-dependent Ca2+ channels, inhibited the secretion induced by trichosporin-B-III (5 microM) in a concentration-dependent manner. Trichosporin-B-III-induced (at 5 microM) secretion also was suppressed by the addition of Mn2+ (5 mM) to the medium. The diltiazem (20 microM) inhibition of trichosporin-B-III-induced (at 5 microM) secretion was reversed by increasing the external Ca2+ concentration. These results indicate that trichosporin-B-III causes the secretion of catecholamines from bovine adrenal chromaffin cells by two mechanisms, Ca2+ dependent and Ca2+ independent (only at high concentrations of trichosporin-B-III). Furthermore, these results strongly suggest that trichosporin-B-III, in Ca(2+)-dependent secretion, activates endogenous voltage-dependent Ca2+ channels, or itself forms the channels in the membranes, and induces Ca2+ influx into the cells.

Adrenal Medulla↗
PubMed1991

[Use of iontophoretic anesthesia for venipuncture].

The usefulness of iontophoretic anesthesia with 10% lidocaine was evaluated on insertion of venous catheters on 38 blood donors in a blood bank and on 41 patients in a hospital, after the arm was charged for 3, 6 or 9 minutes with 1.5 mA of electricity by using a hand-made iontophoretic anesthesia apparatus. In the blood donor group, the pain-relief effect was observed in 25% of donors after charging for 3 min; in 68% after 6 min; and in 93% after 9 min. In the patient group, anesthesia was observed in 14% of patients after 6 min and in 65% after 9 min though the effect was observed in 81% after 6 min and in 65% after 9 min. But only 45-48% of subjects in both groups requested the anesthesia after charging for either 6 or 9 min. This suggests that the duration for 9 min was not liked by the subject despite the pain on insertion. Therefore it is concluded that the charging duration of the iontophoresis must be shorter for this method to become useful as local anesthesia.

Adult↗
PubMed1990

Role of Ca2+/phospholipid-dependent protein kinase in catecholamine secretion from bovine adrenal medullary chromaffin cells.

The role of Ca2+/phospholipid-dependent protein kinase (protein kinase C) in catecholamine secretion from bovine adrenal medullary chromaffin cells was examined using four protein kinase C inhibitors: polymyxin B, sphingosine, staurosporine, and 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H-7). For this purpose, digitonin-permeabilized chromaffin cells were used. Secretion of catecholamines from these cells was stimulated by the addition of micromolar amounts of exogenous free Ca2+. 12-O-Tetradecanoylphorbol-13-acetate (TPA) and arachidonic acid, activators of protein kinase C, enhanced the catecholamine secretion evoked by Ca2+. But phorbol-12, 13-diacetate, a phorbol ester analog that does not activate protein kinase C, had no effect on Ca2(+)-evoked secretion. Polymyxin B at a low concentration (1 microM) abolished the enhancement of secretion by TPA or arachidonic acid without affecting the secretion evoked by Ca2+. However, polymyxin B at higher concentrations (10-100 microM) greatly reduced Ca2+-evoked catecholamine secretion. Sphingosine 10 microM-1 mM), Staurosporine (100 nM-1 microM, and H-7 (100-500 microM) inhibited TPA- or arachidonic acid-enhanced secretion but not Ca2(+)-evoked secretion. In cells in which protein kinase C was down-regulated by TPA, specific binding of [3H]phorbol-12,13-dibutyrate to the cells almost disappeared and the enhancement of secretion by TPA was no longer observed, whereas Ca2(+)-evoked secretion was maintained. These results strongly suggest that protein kinase C is not essential for the Ca2(+)-dependent catecholamine secretion from bovine adrenal chromaffin cells, but acts instead as a modulator.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1989

p-chloromercuribenzoate causes Ca2+-dependent exocytotic catecholamine secretion from cultured bovine adrenal medullary cells.

Incubation of cultured bovine adrenal medullary cells with p-chloromercuribenzoate (50-500 microM), a sulfhydryl-reacting agent, caused an increase in the secretion of catecholamines, p-Chloromercuriphenyl sulfonate, a p-chloromercuribenzoate analogue that poorly penetrates the cell membrane, caused a similar increase in catecholamine secretion. In both cases, catecholamine secretion was dependent on extracellular Ca2+. Furthermore, p-chloromercuribenzoate caused both 45Ca2+ influx into the cells and an increase in the intracellular free Ca2+ concentration. The increases in catecholamine secretion and 45Ca2+ influx behaved similarly in relation to p-chloromercuribenzoate concentration. The time courses of the increased secretion, 45Ca2+ influx, and intracellular free Ca2+ concentration by p-chloromercuribenzoate were also quite similar. The stimulation of catecholamine secretion by p-chloromercuribenzoate was reversed by washing the cells with dithiothreitol-containing medium, but not by dithiothreitol-free medium. When the cells were treated with p-chloromercuribenzoate, dopamine-beta-hydroxylase, an enzyme present in the chromaffin granules along with catecholamines, was also released. However, p-chloromercuribenzoate did not cause release of phenylethanolamine-N-methyltransferase, an enzyme present in the cytoplasm. These results indicate that catecholamine secretion due to p-chloromercuribenzoate occurs by Ca2+-dependent exocytosis.

Adrenal Medulla↗
PubMed1989

[Evaluation of toxic effects on yusho causal substances by chick embryo hepatic microsomal enzymes activities].

PCBs, non-ortho chlorine substituted PCBs (Co-PCBs), PCQs and (PCDFs + PCDDs), all of which contained similar compositions of those corresponding in yusho oil, were prepared from a PCB preparation used as a heat exchanger fluid. After dissolved in 1, 4-dioxane, they were applied into the air sac of white leghorn eggs incubated for 16.5 days at 37.5 degrees C. Forty eight hours after injection, the hepatic benzo(a)pyrene hydroxylase (AHH) and 7-ethoxyresorufin deethylase (EROD) activities were assayed. The average relative potencies of induction for the two microsomal drug metabolizing enzymes by (PCDFs + PCDDs), Co-PCBs, PCBs and PCQs were 100, 13.4, 0.0006 and 0.0004, respectively. The toxic effects for yusho disease by these substances were calculated from the relative enzyme induction potencies and the average concentrations in yusho oils with the production dates of February 9 and 10, 1968. Consequently, the relative toxicities of (PCDFs+PCDDs), Co-PCBs, PCBs and PCQs were 100, 13.2, 0.06 and 0.12, respectively. This result, as well as our previous investigations using rats and monkeys, insists that (PCDFs+PCDDs) are the primary causal agents for yusho disease. However, the Co-PCBs, which were recently detected in the yusho oils by us, were revealed to be fairly effective in yusho manifestation. In addition, it was cleared that the hepatic enzyme induction by the Co-PCBs fraction, which contained other several PCB isomers, was almost completely contributed by only Co-PCBs such as 3,4,3',4'-tetra- 3,4,5,3',4'-penta- and 3,4,5,3',4',5'-hexachlorinated biphenyls present in the fraction. A chemical uptake rate from the air sac by the chick embryo decreased significantly in the cases of extremely high doses of PCBs (10,000 micrograms/egg) and PCQs (3,333 and 10,000 micrograms/egg), and result the elevations of hepatic enzymes activities were depressed, indicating that the suitable chemical dose amount to be less than about 1,000 micrograms/egg.

Animals↗
PubMed1987

Inhibitory effect of polymyxin B on catecholamine secretion from cultured bovine adrenal medullary cells.

Incubation of cultured bovine adrenal medullary cells with 12-O-tetradecanoylphorbol-13-acetate (TPA), an activator of Ca2+/phospholipid-dependent protein kinase (protein kinase C), was associated with increased secretion of catecholamine (CA) from the cells. Polymyxin B (PMB, 30-300 microM), a preferential inhibitor of protein kinase C, inhibited the TPA-induced secretion of CA. PMB also inhibited CA secretion induced by other secretagogues, the Ca2+ ionophore ionomycin (10 microM), 56 mM K+ or acetylcholine (ACh). Ionomycin, 56 mM K+ or ACh increased the concentration of intracellular free Ca2+ ([Ca2+]i) (measured using the fluorescent calcium indicator quin2), whereas TPA did not increase [Ca2+]i. PMB blocked the increase in [Ca2+]i induced by 56 mM K+ or ACh at concentrations similar to those inhibiting the secretion of CA. In contrast, PMB did not affect ionomycin-induced increase in [Ca2+]i. These results strongly suggest that CA secretion induced by TPA or ionomycin is mediated via activation of protein kinase C. The results further indicate that in 56 mM K+- or ACh-evoked CA secretion, PMB inhibits the secretion by blocking Ca2+ influx into the cells.

Acetylcholine↗