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Biomedical subjects

T Muraki

Publications and source records attributed to T Muraki.

At least 145 records · Page 8Linked to original sources
PubMed1980

Adrenergic regulation of blood glucose levels: possible involvement of postsynaptic alpha-2 type adrenergic receptors regulating insulin release.

We have demonstrated that while phenoxybenzamine and prazosin (10(-7)-10(-4) mol/kg i.p.) are ineffective in inhibiting the hyperglycemia induced by alpha adrenergic agonists in fed male mice, phentolamine, yohimbine and dihydroergotamine are effective. These results suggest the involvement of alpha-2 type adrenergic receptors in the regulation of the plasma glucose levels. When attempting to elucidate the mechanism of such differences, we found that the release of immunoreactive insulin induced by epinephrine was markedly stimulated by phentolamine, yohimbine and dihydroergotamine, whereas phenoxybenzamine and prazosin had little effect. The ineffectiveness of these two compounds to inhibit the hyperglycemia induced by alpha adrenergic agonists indicates that the postsynaptic alpha adrenergic receptors which suppress the secretion of immunoreactive insulin from B cells of pancreatic islets are not blocked and that the alpha adrenergic receptors which control immunoreactive insulin secretion differ from the classical postsynaptic alpha adrenergic receptors and more closely resemble presynaptic alpha-2 adrenergic receptors.

Adrenergic alpha-Antagonists↗
PubMed1980

[Narcotic analgesics and endorphins and the release of pituitary hormones (author's transl)].

This report concerns a review of the neuroendocrine effects of narcotic analgesics and endorphins. Acute administration of narcotic analgesics to rats increases the blood levels of ACTH, GH and prolactin, and decreases levels of LH and TSH, however, there is no general consensus regarding changes in serum FSH, ADH and oxytocin as induced by narcotics in rats. In humans, the narcotic analgesic increases in serum prolactin, decreases in serum LH and has no effect on the release of other known pituitary hormones. Endorphins mimic morphine regarding hormonal effects. Effects of naloxone on the basal levels of prolactin, LH or GH were inverse to the effects seen with narcotics and endorphins, therefore endorphins may play a role in regulating the basal levels of these hormones. Narcotics analgesics depress the increased blood levels of prolactin, gonadotropins or TSH elicited by specific measures. While chronic administration of morphine results in tolerance to the stimulant effect of ACTH, and possibly of prolactin secretion, tolerance does not develop to the stimulant effect on GH secretion. The analgesic potency of narcotic analgesics correlates with their suppressive effect on the pituitary-gonadal system and the potency with which endorphins bind to the opiate receptors correlates with their prolactin releasing activity. It is assumed that narcotic analgesics and endorphins exert their hormonal effects by altering the release of neurotransmitters in the CNS. Thus, a release of hypothalamic releasing hormones is involved rather than a direct action on the pituitary. The central neurotransmitter systems involved in the hormonal effects of narcotics are now being intensively investigated by various groups of workers.

Adrenocorticotropic Hormone↗
PubMed1980

Suppressive effect of morphine on serum gonadotropin levels in castrated rats.

A single administration of morphine reduced both serum LH and FSH levels in castrated Wistar rats. As the inhibitory effect of morphine on serum LH was antagonized by naloxone, the opiate receptors are involved. Decrease in the serum FSH levels induced by morphine was considerably less than the decrease in serum LH, and naloxone did not significantly reverse this effect of morphine on serum FSH. Increase in the serum LH induced by exogenous LHRH was slightly potentiated and not inhibited by a large dose of morphine, in both intact and castrated rats. Increase in the serum FSH in intact male rats induced by exogenous LHRH was not altered by morphine. In the castrated animals, exogenous LHRH did not further increase the serum FSH levels and the latter was not altered by a concomitant administration of morphine. These results clearly show that the decrease in serum gonadotropin levels by morphine is not due to inhibition of the stimulatory effect of LHRH on the pituitary gland. The mechanism of the differential suppression on serum LH and FSH by morphine is postulated.

Animals↗
PubMed1979

[A study on the biological action of hypothalamic tridecapeptide, neurotensin (author's transl)].

Investigations on various kinds of biological actions of a newly purified hypothalamic tridecapeptide, neurotensin, were performed both in vivo and in vitro by utilizing experimental animal models. The effect of neurotensin on pituitary gonadotropin release was studied in ovariectomized estrogen-progesterone-treated rats by the measurement of serum levels of luteinizing hormone (LH), follicle stimulating hormone (FSH) and prolactin (PRL) in radioimmunoassays. Neurotensin (340 mg/100 g BW) significantly increased serum LH and FSH 30 minutes after an intravenous injection (p smaller than 0.05) and lowered serum prolactin concentrations significantly (p less than 0.025). Bradykinin and substance P showed on significant effect on serum LH and FSH release. Intraperitoneal or intravenous administration of 0.5 n.mole neurotensin lowered blood pressure in intact mature rats from the range of 90 approximately 100 mmHg to 50 approximately 60 mmHg; however, tachyphylaxis was observed after repeated injections of the same dose of this peptide. Neurotensin was as potent as bradykinin in inducing rat duodenum relaxation and guinea pig ileum contraction in vitro. Theses effects on neurotensin and bradykinin on the intestines were not inhibited by the pre-treatment of phentolamine, propranolol, methysergide and pyribenzamine. Bradykinin induced contractions of the uterus in proestrous rats, but neurotensin induced no marked contraction. These results suggest that neurotensin in not hypothalamic releasing or inhibiting factor but possess the nature of kinin.

Animals↗
PubMed1979

Inhibition by cholinergic agonists of the prolactin release induced by morphine.

The cholinergic agonists, pilocarpine, physostigmine and nicotine, inhibited the prolactin release induced by morphine in male rats in vivo. Pilocarpine also inhibited the release of prolactin induced by beta-endorphin or metoclopramide without affecting the basal and haloperidol-stimulated serum prolactin levels. The inhibitory effect of pilocarpine on the morphine-stimulated release of prolactin was antagonized by concurrent administration of atropine but not by atropine methylnitrate or by mecamylamine, while the inhibition by nicotine was antagonized by mecanylamine but not by atropine. The stimulation of prolactin release by morphine and its reversal by pilocarpine were observed after the administration of haloperidol or alpha-methyltyrosine. These results suggest that the central cholinergic system exertes an inhibitory influence on the prolactin release induced by morphine or beta-endorphin and the cholinergic inhibition is not mediated via catecholaminergic neurons.

Animals↗
PubMed1979

Effect of narcotic analgesics and naloxone on proestrous surges of LH, FSH and prolactin in rats.

Morphine (50 mg/kg), given at 12:00 h and 14:00 h to proestrous rats, completely inhibited the proestrous surges of serum luteinizing hormone (LH), follicle-stimulating hormone (FSH) and prolactin (Prl). However, when it was given at 16:00 h, the inhibitory effect of morphine (Mor) was decreased. Pethidine and nalorphine inhibited the proestrous surges, while pentazocine showed a weaker inhibitory effect. Naloxone (Nx), given simultaneously or 2 h after morphine (Mor), at 1/20 the dose of Mor, inhibited the blockade of the proestrous gonadotropin release exerted by Mor, while the onset of the surges was delayed when it was given 3 h after Mor.

Analgesics, Opioid↗
PubMed1979

Inhibitory effects of corticosterone on cell proliferation and steroidogenesis in the mouse adrenal tumor cell line Y-1.

Monolayer cultures of mouse adrenal tumor cell line Y-1 have been used to investigate the effects of glucocorticoid on cell replication, [3H]thymidine incorporation into the trichloroacetic acid-precipitated cell fraction, steroidogenesis, and the ACTH receptors of adrenocortical cells. Corticosterone at a concentration of 5.0--50 micrograms/ml inhibited cell replication and [3H]thymidine incorporation into trichloroacetic acid-precipitated cell fraction in a dose-related manner. Corticosterone at a concentration of 0.5--50 micrograms/ml inhibited ACTH-induced steroidogenesis in a dose-related manner. Steroids which do not possess glucocorticoid action did not show such inhibitory effects on cell replication and steroidogenesis of Y-1 cells. The characteristics of the ACTH receptors of these cells remained unaffected by corticosterone. Our findings suggest that synthesized or secreted glucocorticoid may play an important role in the direct regulation of proliferation and function of adrenocortical cells under physiological conditions.

Adrenal Gland Neoplasms↗
PubMed1978

Effects of morphine on the serum prolactin levels of morphine-tolerant and nontolerant male rats and of the in vitro release of pituitary prolactin.

Morphine increased the serum prolactin (PRL) levels of male rats in a dose response manner. This effect was abolished by naloxone and apomorphine, but was not affected by diphenhydramine. The increase in the serum PRL levels by haloperidol was abolished by apomorphine, but not by naloxone. Repeated administrations of increasing doses of morphine attenuated the response of serum PRL to morphine. Naloxone did not alter the serum PRL levels of morphine-tolerant rats, while it precipitated full withdrawal signs on these rats. Although neither haloperidol nor morphine increased the release of PRL from the isolated anterior pituitary, haloperidol, but not morphine, reversed the inhibition by dopamine of the in vitro release of pituitary PRL. These results indicate that tolerance develops regarding the effect of morphine with a resulting increase in the serum PRL levels, abstinence precipitated by naloxone has no effect on the serum PRL levels, the mechanism of morphine involved in increase in the serum PRL is different from that of haloperidol as the effect of haloperidol is not antagonized by naloxone and morphine does not antagonize the effect of dopamine which inhibits the release of PRL from the anterior pituitary in vitro.

Animals↗
PubMed1978

Time course of effects of morphine on hypothalamic content of LHRH and serum testosterone and LH levels of morphine-tolerant and nontolerant male rats.

Time course of the effects of morphine on the hypothalamic content of LHRH in both nontolerant and morphine-tolerant male rats was investigated in relation to the temporal changes of serum testosterone and LH levels. The hypothalamic LHRH content of the nontolerant rats was increased 8 hr after the administration of morphine (100 mg/kg) when serum testosterone levels were depressed. The LHRH content of the tolerant rats was decreased during withdrawal of morphine for 48 hr when the lowered serum testosterone and LH levels had returned to within the control levels. Although the hypothalamic LHRH content does not necessarily reflect the release of LHRH, these results are in favour of the hypothesis that the release of hypothalamic LHRH is inhibited by the administration of morphine and is restored by the withdrawal of the narcotic.

Animals↗
PubMed1977

Intestinal responses to hyperosmolar glucose infusion in dogs.

Physiological and morphological changes of small intestine after hyperosmolar glucose infusions into canine jejunum were studied using in vivo perfusion model. Infusions of 40 ml of 50% and 20% glucose solution into the jejunal loops induced biphasic osmolar degression in the lumen. Osmolarity of jejunal venous blood was rapidly increased and maintained the maximal level (approximately 320 mOM/L). Blood flow to the jejunal loop was significantly increased after 50% glucose infusion compared to 5% glucose infusion. Most characteristic electron microscopic change of jejunal epithelial cell was pseudo-pod like process projected into the jejunal lumen, which was very similar to that of cholera.

Acetylcholine↗
PubMed1977

Effects of repeated morphine administration on copulation and on the hypothalamic-pituitary-gonadal axis of male rats.

Adult male rats were administered morphine twice a day for 45 days and the effects of morphine on the copulation rate, the weight of various organs, and on the hypothalamic-pituitary-gonadal axis were examined. Morphine administered rats showed a loss of weight, hypertrophy of the adrenals, decreased weight of accessory sex organs, low sperm count, and decreased copulation rate. The contents of the luteinizing hormone releasing hormone in the hypothalamus and the luteinizing hormone in the pituitary remained unchanged. Serum luteinizing hormone and testosterone levels decreased, but serum follicle-stimulating hormone levels increased. These results suggest that morphine inhibits the hypothalamic-pituitary-gonadal axis and causes a diminution in the number of fertilizations of the partner females.

Animals↗
PubMed1977

Effects of morphine and naloxone on serum LH, FSH and prolactin levels and on hypothalamic content of LH-RF in proestrous rats.

Proestrus surges of serum LH, FSH and prolactin (PRL) were significantly reduced when morphine HCl (50 and 10 mg/kg) was administered to 4-day cycling rats just prior to the proestrous critical period. The inhibitory effect of morphine was reversed by naloxone, a morphine antagonist, at the dose which had no effect on the proestrus surges of serum LH, FSH or PRL. The hypothalamic LH-RF content of proestrous rats at 1800 hr (during the proestrus surge) was not significantly different from that at 1400 hr (before the surge) and was not affected by pretreatment with morphine or naloxone. Our results suggest that naloxone reverses the anti-ovulatory effect of morphine by antagonizing the inhibitory effect of morphine on preovulatory surges of gonadotropins or PRL.

Animals↗
PubMed1976

Presence of TSH receptor in thyroid neoplasms.

The nature of the TSH receptor in adenoma and carcinoma of the thyroid gland was studied using a radioreceptor assay technique. A membrane fraction of tissue homogenate was obtained by discontinuous sucrose gradient ultracentrifugation, and 125I-TSH, labelled by a lactoperoxidase method, was purified with a receptor adsorption method. Both the capacities and the association constants of high affinity receptors (4 x 10(9) M-1) and of low affinity receptors (0.073 x 10(9) M-1) observed in the normal thyroid were almost identical to those of the thyroid of Graves' disease and those of thyroid adenoma. Although the two papillary carcinomas examined were found to have two kinds of TSH receptors, one of the carcinomas showed decreased association constants for both high affinity and low affinity receptors.

Adenoma↗