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Biomedical subjects

M Oka

Publications and source records attributed to M Oka.

At least 739 records · Page 41Linked to original sources
PubMed1980

Enhanced vascular reactivity to various vasoconstrictor agents following pinealectomy in the rat: role of melatonin.

The mesenteric vascular bed preparation of control and pinealectomized (PX) male Wistar rats was used to examine vascular reactivity to two concentrations each of norepinephrine, serotonin, angiotensin, and potassium. Vasoconstrictor responses to 50- and 100-ng injections of norepinephrine and 0.5- and 1.0-microgram injections of serotonin were 30-40% higher in preparations from PX rats. Reponses to 100 ng but not to 50 ng of angiotensin were also significantly higher in preparations from PX rats. Responses to 1.5- and to 3.0-mg injections of potassium did not differ significantly in either case. In vivo injection of 20 microgram of melatonin 3 h prior to dissection of the preparation, or in vivo perfusion of 20 ng melatonin per millilitre of buffer completely reversed the increased vascular response to all vasoconstrictor agents tested in the PX preparations, but had little effect in control preparations. Also observed in PX rats was a significant increase in blood pressure, serum sodium, and increased body and heart weight. Arterial wall sodium was also elevated in PX rats. These changes may be relevant to the increased vascular reactivity of PX rats. The increased vascular responsiveness of PX rats may be specific for agents that stimulate calcium release from intracellular stores (norepinephrine, angiotensin) rather than those that stimulate calcium influx from extracellular fluid (potassium). Melatonin lack may be the cause of the vascular changes in the PX rats as both in vivo and in vitro it lowered the vasoconstrictor effects of the agents tested, but only in PX rats; it had no significant effect in the control rats.

Angiotensin II↗
PubMed1980

Effect gamma-melanotropin (gamma-MSH) on the conditioned behavior.

Effects of a dodecapeptide containing the gamma-MSH sequence on two types of conditioned behaviors were investigated. This peptide enhanced the avoidance response in poorly-performing mice, while it suppressed the self-stimulation lever pressing in rats. At higher doses, the peptide induced slight convulsions of a myoclonic type. The significance of these behavioral changes has not been assessed, but the results suggest that gamma-MSH may have some physiological function in the central nervous system.

Amino Acid Sequence↗
PubMed1980

Avoidance enhancement and discriminative response control by anxiolytics with drugs acting on the GABA system.

Two types of conditioned behaviors were investigated for the purpose of evaluating anxiolytic drugs. A conditioning procedure used was an active avoidance in poorly-performing mice. Chlordiazepoxide, diazepam, chlorazepate and meprobamate increased the avoidance rate, while chlorpromazine, haloperidol and nortriptyline did not produce such an effect. The effect of diazepam was potentiated by gamma-aminobutyric acid (GABA) and aminoxyacetic acid (AOAA) and antagonized by picrotoxin and thiosemicarbazide, but was influenced little by spiroperidol, alpha-methyltyrosine, phenoxybenzamine and levallorphan. In addition, the effect of other anxiolytics was potentiated by AOAA and antagonized by picrotoxin. Biperiden, methamphetamine, caffeine and morphine also induced an avoidance enhancement, which was not influenced by AOAA. A drug discrimination experiment was also performed using a milk-reinforced two-lever operant method. In the rats trained to discriminate phenobarbital from saline, diazepam produced a dose-related phenobarbital-lever selection, which was potentiated by AOAA and antagonized by picrotoxin. Chlordiazepoxide, chlorazepate and meprobamate also elicited responses on the phenobarbital-lever. On the other hand, haloperidol, nortriptyline, biperiden, methamphetamine, caffeine and morphine produced a saline-lever selection, at the doses tested. These results suggest that, among several drugs tested, the avoidance enhancement and discriminative response control by anxiolytics may be closely linked with the GABA system.

Aminooxyacetic Acid↗
PubMed1980

Mechanism of renin inhibition by beta adrenergic blocking agents. Effects of dl-, d-, l-propranolol and pindolol on renin release.

In order to reveal the mechanism of renin inhibition by beta adrenergic blocking agents, the effects of dl-, d-, l-propranolol and pindolol on renin release were studied. This was done by injecting them intraperitoneally or by using an in vitro system of rat kidney slices. In the in vivo study, dl-, d-, and l-propranolol inhibited plasma renin activity and renal renin content significantly in normal rats. Furthermore, in the in vitro study, the basal levels of renin in the media and that in the kidney were significantly inhibited by these agents. Pindolol also inhibited renin release, but its effects were significantly less than those of other agents. The finding that d-propranolol which has little beta adrenergic blocking action inhibited renin release, and that the effects of pindolol which displays strong beta adrenergic blocking action but little membrane stabilizing action, were less than those of other agents, may suggest that the inhibitory effects of beta adrenergic blocking agents on renin release are dependent mainly on the membrane stabilizing action rather than the beta adrenergic blocking action.

Adrenergic beta-Antagonists↗
PubMed1980

A method for quantitation of vitamin B2 by using an enzyme (producing vitamin B2-aldehyde) from Schizophyllum commune.

A method for enzymatic determination of riboflavin was developed by enzymatic reduction of 2,6-dichlorophenolindophenol using a vitamin B2-aldehyde-forming enzyme prepared from Schizophyllum commune. The enzymatic method enabled us to determine riboflavin in a mixture containing riboflavin, FMN and FAD without separation of riboflavin. Moreover, the total amount of flavins in the mixture was shown to be determined by the enzyme in the presence of phosphatase.

2,6-Dichloroindophenol↗
PubMed1980

Inhibitory action of morphine on the release of a bradykinin-like substance after sciatic nerve stimulation.

Effects of morphine on the release of a bradykinin-like substance into the subcutaneous perfusate of the rat paw, elicited by pinching and heating of the foot instep and by electrical stimulation of the sciatic nerve, were investigated. Morphine (5 mg/kg i.m.) inhibited the release of a bradykinin-like substance only when sciatic nerve stimulation was applied. The release due to sciatic nerve stimulation was not inhibited by gallamine (8 mg/kg i.p.), but significantly by physostigmine (1 mg/kg i.p.). The release was also observed by adrenergic agents and was inhibited by adrenergic alpha-blocking agents. No release of a bradykinin-like substance due to sciatic nerve stimulation was observed in reserpinized and 6-hydroxydopaminized rats. Dopa restored the releasing ability due to sciatic nerve stimulation in the reserpinized rats, but not in the 6-hydroxydopaminized ones. The results suggest that the inhibitory action of morphine can be explained by an inhibition of the release of noradrenaline.

Animals↗
PubMed1979

Significance of adrenergic alpha-effect on salivary kallikrein secretion in the submandibular gland of the dog.

The effects of the sympathetic nerve stimulation and the administrations of sympathomimetics on the secretion of salivary kallikrein induced by the chorda tympani stimulation were examined quantitatively and qualitatively in the submandibular gland of the dog. The secretion of salivary kallikrein may be mediated through both adrenergic alpha- and beta-receptors. The activities of salivary kallikrein secreted by either the chorda tympani stimulation or isoproterenol were not inhibited by soy bean trypsin inhibitor in vitro, but those secreted by the sympathetic nerve stimulation and noradrenaline or adrenaline were markedly inhibited in vitro. These results suggested that secretion of glandular kallikrein was induced by the chorda tympani stimulation and the sympathetic beta-stimulation, and secretion of plasma kallikrein was induced by the sympathetic alpha-stimulation.

Animals↗