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Biomedical subjects

M Wakui

Publications and source records attributed to M Wakui.

87 records · Page 5Linked to original sources

Decrease in membrane conductance induced by noradrenaline in the smooth muscle of guinea-pig vas deferens.

The electrical response of the smooth muscle of guinea-pig vas deferens to exogenously applied noradrenaline (NA) was examined using the double sucrose-gap method. NA evoked a depolarization of the smooth muscle membrane which was associated with an increase in the size of electrotonic potentials. A conditioning depolarization of the membrane induced by current application enhanced the size of NA-induced depolarization, whereas a conditioning hyperpolarization reduced it. When a conditioning hyperpolarization of 25 mV in magnitude was applied, the direction of potential change induced by NA was reversed. These results are discussed with respect to the ionic mechanism of the electrical event in response to NA in this tissue.

Adenosine Triphosphate↗

Evidence for an increase in membrane conductance during adenosine triphosphate-induced depolarization in the guinea-pig vas deferens.

The effects of exogenously applied adenosine triphosphate (ATP) on the smooth muscle of guinea-pig vas deferens were studied with the double sucrose-gap method. ATP evoked a membrane depolarization which was associated with a decrease in the size of electrotonic potentials. Conditioning hyperpolarization induced by current application caused an increase in the magnitude of the ATP-induced depolarization; the larger the conditioning hyperpolarization, the greater the ATP-induced depolarization. These results are discussed with respect to the ionic mechanism of the electrical event in response to ATP in this tissue.

Adenosine Triphosphate↗

Inhibitory effect of methylmercuric chloride on the contraction mediated by muscarinic receptor of intestinal smooth muscle of the guinea-pig.

Effects of methylmercuric chloride (MMC) on the contractile responses to nerve and drug stimulation in the guinea-pig taenia coli were examined. MMC (25-50 microM) severely reduced both responses to electrical and pharmacological (nicotine) stimulation of cholinergic nerves without affecting the responses to direct stimulation of muscles. MMC also suppressed markedly the response to acetylcholine (ACh), but did not change the maximum response to ACh. Dose-inhibition curve for MMC on the response to nerve stimulation was quite similar to that on the response to externally applied ACh. MMC only at a high concentration slightly reduced the response to histamine. MMC depolarized the membrane of the smooth muscle by about 8 mV with the sucrose-gap method. However, conditioning depolarization of the muscle strip by a 25 mM-K solution did not suppress the response to ACh. It was suggested that MMC-induced inhibition of the responses of the guinea-pig taenia coli to cholinergic nerve stimulation resulted from the inactivation of the muscarinic receptor of the smooth muscle.

Acetylcholine↗

Requirements of external Ca and Na for the electrical and mechanical responses to noradrenaline in the smooth muscle of guinea-pig vas deferens.

Noradrenaline (NA) evoked a contraction which consisted of two components, an initial one associated with only depolarization and a second one with spike discharges. Both contractions were abolished in a Ca-free solution leaving only small depolarization. In a Na-free solution, the initial contraction was increased in keeping with the short term depolarization, while the second contraction was abolished. It is suggested that NA initially causes Ca influx which secondarily increases Na permeability.

Animals↗

Electrical and mechanical events through activation of muscarinic receptor in the smooth muscle of guinea-pig vas deferens.

Electrical and mechanical responses of the guinea-pig vas deferens to exogenous acetylcholine (ACh) were observed by means of a single sucrose-gap method. ACh at various concentrations evoked a contraction consisting of two components. The initial component seemed to be independent of a depolarization, while the second one was dependent on it. All ACh responses were abolished by Ca removal from the external solution. The results suggest the existence of a pathway by which ACh even at low concentrations causes a Ca influx without potential changes.

Acetylcholine↗

In vivo staining test with methylene blue for bladder cancer.

An in vivo staining test with 0.2 per cent methylene blue was applied to 129 patients with bladder tumor and 16 patients with chronic cystitis within a 6-year interval. Although normal mucosa did not pick up the stain nonpapillary in situ and microinvasive carcinomas did so frequently. Moderate dysplasia was stained in about half of the patients. The intensity of the stain in papillary tumors was correlated with the histologic anaplasia (grade). Grade 1 tumors were stained poorly or unstained in 86 per cent of the tests, whereas grades 2 and 3 tumors picked up the stain in 74 and 96 per cent of the tests, respectively. Even a tiny tumor, if poorly differentiated, was identified easily by the blue stain. The histologic anaplasia of tumors could be assessed roughly according to the intensity of the stain. However, chronic cystitis occasionally took up the stain, especially in cases of marked inflammatory infiltrate a deep stain was recognized. To differentiate nonpapillary early cancer from chronic cystitis the addition of a cytologic examination may be necessary.

Biopsy↗

Effect of cobalt on electrical and mechanical responses to exogenous noradrenaline and to field stimulations in the guinea-pig vas deferens.

Co2+ suppressed the mechanical responses evoked by field stimulations and by application of noradrenaline (NA) in the smooth muscle of guinea-pig vas deferens. However, the membrane excitation and force development evoked by depolarizing currents were not much affected in the Co2+ treatment. It is proposed that Co2+ suppresses NA induced contraction by inhibiting the development of the membrane depolarization.

Action Potentials↗

[Combination chemotherapy with bleomycin, vincristine and methotrexate for stage I non-seminomatous germ cell testicular tumors].

Ten patients with Stage I non-seminomatous germ cell testicular tumors underwent orchiectomy and combination chemotherapy with bleomycin, vincristine and methotrexate with CF rescue (BOM) as an induction therapy followed by cyclophosphamide, vincristine and methotrexate as a maintenance therapy (COM). The results were as follows: BOM seemed to be effective as a further treatment for Stage I non-seminomatous germ cell testicular tumor patients. All 10 patients are alive and disease-free for a period from 1 year and 6 months to 5 years and 3 months (mean: 3 years and 9 months). The chemotherapy should be continued at least for a year, since relapse occurred in 2 of 4 patients who received only induction therapy. However, they completely responded to other chemotherapy regimens (BVP and BOAM ). BOM and COM therapy were scarcely toxic and no serious side effects were recognized. From the above results, it was considered that combination chemotherapy (BOM and COM) can be an alternative treatment to the conventional retroperitoneal node dissection and radiation therapy for Stage I non-seminomatous germ cell tumors.

Adult↗

[Primary multiple malignant tumors associated with bladder cancer].

Of 487 patients with urothelial bladder cancer seen during the past 22 years, 37 (7.6%) had other primary malignant tumors. In recent years the number of patients with double cancer markedly increased. The male/female ratio was 2.7:1 and the mean age at the time of diagnosis of the second primary cancer was 70 (56-84) years. Of the other organ cancers, 18 (47%) were in the digestive tract and 7 (18%) in the respiratory tract. Six patients had lesions that were diagnosed simultaneously and 31 had lesions that were diagnosed at intervals. The interval in 31 patients with metachronous double cancer ranged from 1 year and 1 month to 40 years; the mean interval was 9 years and 7 months.

Age Factors↗

ACh-evoked complex membrane potential changes in mouse submaxillary gland acini. A study employing channel blockers and atropine.

The responses in membrane potential and resistance of acinar cells to iontophoretically applied acetylcholine (ACh) were investigated using intracellular micro-electrode recording in superfused segments of mouse submaxillary gland. For measurements of membrane resistance and acetylcholine equilibrium potential (EACh), two micro-electrodes were inserted into neighbouring communicating cells. Current could be injected through one of the electrodes. The pattern of membrane potential change induced by ACh depended on the resting potential. Simple hyperpolarizations were induced at low resting potentials, while biphasic potential changes (depolarization followed by hyperpolarization) or simple depolarizations were observed at relatively high resting potentials. A similar dependence of the ACh induced potential change on the resting potential was obtained in experiments in which the resting membrane potential was set at different levels by injecting direct current and stimulating the same cell with equal doses of ACh. The ACh equilibrium potential ranged widely between -45 and -75 mV. Under special conditions the conversion in response to ACh from a hyperpolarization to depolarization could be obtained without change in resting potential. Small doses of ACh evoked simple depolarization, while medium doses induced biphasic responses and large doses of ACh caused hyperpolarization. The effect of a low concentration of atropine on the response was an initial block of hyperpolarization followed by a secondary block of depolarization. Intracellular injection of TEA ions converted the ACh induced potential response from hyperpolarization to depolarization. Both the depolarizing and hyperpolarizing ACh responses were accompanied by a marked reduction in membrane resistance. The depolarization was abolished by a severe reduction in external Na concentration, while the hyperpolarization was sensitive to alternations in external K concentration. These results indicate that some of the complex responses in submaxillary gland acinar cells to ACh may be explained by the interaction between two different kinds of potential change (Na dependent depolarization and K dependent hyperpolarization).

Acetylcholine↗

Effect of neural stimulation on acinar cell membrane potentials in isolated pancreas and salivary gland segments.

The effect of cholinergic neural excitation by field stimulation on the acinar cell membrane potential was investigated in superfused segments of mouse pancreas and salivary glands (sublingual, submaxillary, and parotid glands). Responses of acinar cells in both exocrine pancreas and salivary glands to the neural excitation obtained by field stimulation were similar to responses previously described in each gland to the externally applied acetylcholine. In the pancreatic acinar cell, electrical field simulation induced depolarization with a latency of 0.3 to 1.2 sec. This depolarization was accompanied by a marked decrease in membrane resistance. The equilibrium potential of the depolarization induced by stimulation was between - 10 and - 20 mV. In the sublingual gland, field stimulation induced depolarization of the acinar cell with a latency of 0.2 to 0.3 sec. The stimulus induced depolarization was block by the addition of atropine. In the submaxillary and parotid glands, field stimulation induced depolarization in some acinar cell and hyperpolarization in other cells. The results support evidence previously presented by Petersen and his colleagues that acetylcholine acts to increase Na+ and K+ or Na+, K+, and Cl- permeabilities in the pancreatic acinar cell and to increase K+ and Na+ permeabilities in the salivary gland [11,24].

Acetylcholine↗

Effect of neural stimulation on contractile system (myoepithelial cells) in isolated salivary gland segments of rat.

The effect of cholinergic neural excitation by field stimulation on the tension of the contractile system (myoepithelial cells) was investigated in superfused segments of rat salivary glands (sublingual, submaxillary, and parotid). Electric field stimulation evoked gland tissue contraction of a few mg, which was blocked by addition of TTX or atropine. The order of the magnitude of the contraction per wet tissue weight was sublingual greater than submaxillary greater than parotid. This correlates with the order of the distribution of myoepithelial cells described in morphological investigations. Cholinergic stimulants induced contraction in all salivary glands, but adrenergic stimulants hardly evoked contraction in the sublingual gland, whereas those drugs evoked a considerable amount of contraction in the submaxillary gland. These findings seem to suggest that the contraction may originate in the myoepithelial cells. The omission of Na from the superfusing solution quickly abolished the contraction evoked by field stimulation but not the contraction induced by ACh. The omission of Ca from the solution reduced the contraction evoked not only by field stimulation but also by ACh and by high K. The results suggest that extracellular Ca is important for the initiation of myoepithelial contraction.

Acetylcholine↗

Receptor-activated cytoplasmic Ca2+ oscillations in pancreatic acinar cells: generation and spreading of Ca2+ signals.

Receptor-activated cytoplasmic Ca2+ oscillations have been investigated using both single cell microfluorometry and voltage-clamp recording of Ca(2+)-dependent Cl- current in single internally perfused acinar cells. In these cells there is direct experimental evidence showing that the ACh-evoked [Ca2+]i fluctuations are due to an inositol trisphosphate-induced small steady Ca2+ release which in turn evokes repetitive Ca2+ spikes via a caffeine-sensitive Ca(2+)-induced Ca2+ release process. There is indirect evidence suggesting that receptor-activation in addition to generating the Ca2+ releasing messenger, inositol trisphosphate, also produces another regulator involved in the control of Ca2+ signal spreading. Intracellular inositol trisphosphate or Ca2+ infusion produce short duration repetitive spikes confined to the cytoplasmic area close to the plasma membrane, but these signals can be made to progress throughout the cell by addition of caffeine or by receptor activation.

Animals↗