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Biomedical subjects

T Muraki

Publications and source records attributed to T Muraki.

At least 127 records · Page 7Linked to original sources
PubMed1982

Inhibitory alpha 2-adrenergic mechanism regulating gastric secretion in pylorus-ligated rats.

Several alpha-adrenoceptor agonists given intracerebroventricularly or subcutaneously to rats were assessed for their effects on gastric secretion under condition of pylorus ligation. Intracerebroventricular injection of alpha-adrenoceptor agonists reduced gastric secretion, in the following order (relative potency, clonidine = 1): oxymetazoline (100) greater than clonidine (1) greater than methoxamine (0.024) greater than phenylephrine (0.003). The antisecretory effects of oxymetazoline and clonidine given intracerebroventricularly were antagonized with yohimbine administered by the same route. Subcutaneous injection of alpha-adrenoceptor agonists also reduced gastric secretion, in the following order (relative potency, clonidine = 1): clonidine (1) greater than oxymetazoline (0.3), much greater than phenylephrine (0.001) approximately methoxamine (0.0006). Oxymetazoline, when given intracerebroventricularly, was most effective in decreasing the volume and titratable acidity of gastric secretion. Pretreatment with 6-hydroxydopamine intracerebroventricularly (250 micrograms/rat x 2; 72 and 120 h before) reduced the antisecretory effect of clonidine given intracerebroventricularly. Thus, gastric secretion appears to be regulated in an inhibitory manner by alpha 2-, but not by alpha 1- adrenoceptors in the central and peripheral nervous systems, in pylorus-ligated rats.

Adrenergic alpha-Agonists↗
PubMed1982

Partial isolation and characterization of bromosulphosphthalein-binding protein from rat liver plasma membranes.

Digestion of liver plasma membranes with trypsin and chymotrypsin prevented specific binding of 35-S or 131-I-bromosulphophthalein (BSP) to these membranes, in contrast concomitant appearance of BSP binding protein was observed in a high-speed (100,000 x g. 1 hr) supernatant of the extracts. On the other hand, BSP binding capacity of receptors was hardly destroyed by digestion with high concentration of phospholipase A, C. Gel filtration experiments on a column of Sephadex indicated that specific BSP binding to a protein in the high-speed supernatant was observed and this protein contained at least sialic acid and pentose suggesting a fragment of glycoprotein. In addition this molecular size was far smaller than 23,000, calibrated with bovine trypsin. Competitive inhibition was also observed between 131-I-BSP and BSP on a specific protein by gel filtration, while cholic acid did not affect its capacity to bind 131I-BSP. These results suggest that the specific protein on the liver plasma membrane is involved in the transport of organic anions across hepatocyte surface membranes.

Animals↗
PubMed1982

A morphologic study of the behavior of biogenic amines in experimental acetic acid gastric ulcer.

Morphological observations were made of the behavior of biogenic amines in the gastric wall of rats with acetic acid-induced ulcer. In the normal rat stomach, abundant adrenergic fibers were seen in the adventitia of arteries and arterioles, with frequently distributed mast cells in their environs, in all gastric wall layers. Mast cells had a more frequent distribution in the antral region than in the corpus ventriculi while enterochromaffin-like cells (EC-like cells) were found with greater frequencies in the latter region of gastric wall. Adrenergic fibers were abundant around blood vessels in perilesional area of the gastric wall of rats with acetic acid ulcer. Mast cells, seen more frequently in the antral region as in the normal rats, showed degranulation in these rats. The population of PAS-positive mucous cells reached its peak in 10 days after injection of acetic acid and subsequently declined with healing of the ulcer, thus remarkably concordant with the ulcer index. Local administration of serotonin produced angiospasm in the greater omentum. The finding indicates a possible participation of arteriospasm by adrenergic nerve fibers in the pathogenesis of gastric ulcer. The results of the present study strongly suggest that biogenic amines have bearing as an aggressive factor upon the angiospasm theory of ulcerogenesis.

Acetates↗
PubMed1982

Involvement of alpha 1-adrenergic receptors in the inhibitory effect of catecholamines on the thyrotropin-induced release of thyroxine by the mouse thyroid.

TSH enhanced the release of T4 from the mouse thyroid incubated in vitro. Norepinephrine, a nonspecific alpha-adrenergic agonist, and methoxamine, an alpha 1-agonist, inhibited the TSH-stimulated release of T4 at 10(-4) and 10(-5) M, whereas clonidine, an alpha 2-agonist, exerted a weak inhibition. The inhibitory effect of 10(-5) M norepinephrine on the T4 release stimulated by TSH was prevented by prazosin, an alpha 1-antagonist, at concentrations higher than 10(-7) M, whereas yohimbine, an alpha 2-antagonist, exerted weak activity in antagonizing the inhibition induced by norepinephrine. Norepinephrine, methoxamine, and clonidine did not significantly reduce the cAMP accumulation stimulated by TSH in the mouse thyroid incubated in vitro. These findings in the mouse thyroid indicate that catecholamines act by way of alpha 1-adrenergic receptors to suppress TSH-stimulated release of T4 without reducing the cAMP levels stimulated by TSH in the mouse thyroid.

Animals↗
PubMed1981

Adrenergic receptors and the onset of streptozotocin-induced diabetes in mice.

Treatment with yohimbine, an alpha 2-adrenergic blocker, prior to the injection of a subdiabetogenic dose of streptozotocin (STZ) produced hyperglycemia and hypoinsulinemia in mice 7 days later. Prazosin, an alpha 1-adrenergic blocker, was ineffective. The capacity of phentolamine and phenoxybenzamine to potentiate the diabetogenic effect of STZ was intermediate between that of yohimbine and prazosin. Propranolol and hexamethonium inhibited the potentiating action of yohimbine. Yohimbine enhanced the potentiating effect of isoproterenol on the STZ-induced diabetes. Acute changes in phase glucose and insulin levels induced by STZ were potentiated by yohimbine but not by prazosin. The insulin releasing ability of the pancreatic islets 7 days after STZ was all but lost in mice pretreated with yohimbine but not with prazosin. These results suggest that the beta- and alpha 2-, not alpha 1-adrenergic system which modulates insulin release from pancreatic islets influences the response to the diabetogenic action of STZ in mice.

Adrenergic alpha-Antagonists↗
PubMed1981

Thyrotropin (TSH) receptor and adenylate cyclase activity in human thyroid tumors: absence of high affinity receptor and loss of TSH responsiveness in undifferentiated thyroid carcinoma.

TSH receptor and adenylate cyclase activity of plasma membrane fractions of human thyroid tumors were examined. The mean (+/- SD) basal adenylate cyclase activity in normal thyroid tissues was 0.35 +/- 0.33 nmole/mg protein x 10 min. The activity rose to 280% (range, 270-310%) of basal with TSH (166 mU/ml). In adenomas, the activity rose to 600% (range, 530-650), which was significantly higher than that of normal thyroid (P < 0.005). In the differentiated carcinoma, TSH responsiveness of adenylate cyclase was heterogenous (range, 110-520), but was qualitatively similar to that of the normal thyroid. On the other hand, basal adenylate cyclase activity of undifferentiated carcinoma was significantly lower than that of normal thyroid (0.018 +/- 0.007 nmol/mg protein x 10 min; P < 0.05) and was not stimulated by TSH. LH, FSH, and ACTH did not stimulate the enzyme in either kind of carcinomas. The mean (+/- SD) of the capacity of the high affinity receptor of adenomas (0.72 +/- 0.64 pmol/mg protein) and differentiated carcinomas (0.77 +/- 0.84) was not significantly different from that of normal thyroid (0.92 +/- 0.84). The affinity constants of the receptors in these three tissues were much the same (1.6-2.4 x 10(10) M-1). On the other hand, high affinity receptor could not be detected in all of the undifferentiated thyroid carcinoma. It seems likely that the failure of adenylate cyclase to respond to TSH in undifferentiated carcinoma of the thyroid is due to an alteration at the level of the receptor site. These data suggest that growth and metabolic activity of undifferentiated carcinoma may be independent of TSH, while those of adenoma and differentiated carcinoma may be affected by TSH.

Adenoma↗
PubMed1981

Partial agonistic action of morphine in the rat vas deferens.

Effects of morphine on the force of contraction of rat vas deferens were investigated. Morphine and beta-endorphin decreased the electrically evoked twitch tension, in a dose dependent manner. The inhibitory effect of morphine, however, was much weaker than that of beta-endorphin. These effects of both morphine and beta-endorphin were completely antagonized by naloxone. In the presence of 30 microM morphine, the dose-response curve of beta-endorphin shifted to the right by about 10-fold. Moreover, morphine partly reversed the contraction depressed by 0.3 microM beta-endorphin, in a dose dependent manner. These findings suggest that morphine acts as a partial agonist on the rat vas deferens. Marked tolerance to beta-endorphin and change in the antagonist potency of morphine were not observed in the vas deferens isolated from morphine-dependent rats.

Animals↗
PubMed1980

Regulation of plasma insulin level by alpha 2-adrenergic receptors.

Phentolamine, yohimbine or dihydroergotamine markedly increased plasma immunoreactive insulin (IRI) and inhibited epinephrine-induced hyperglycemia in fasted mice. On the other hand, phenoxybenzamine or prazosin only slightly increased plasma IRI and enhanced epinephrine-induced hyperglycemia. These results indicate that there is a distinct difference in the effects of alpha-adrenergic blockers on the plasma IRI and glucose levels, and that alpha-adrenergic receptors responsible for the plasma IRI level resemble alpha 2-adrenergic receptors more closely.

Adrenergic alpha-Agonists↗
PubMed1980

Mechanism of chlorpromazine action on plasma glucose and cyclic AMP levels.

The s.c. administration of chlorpromazine (CPZ) caused an elevation of plasma glucose and cyclic AMP levels in fed intact mice, but not in fed adrenalectomized mice. The pretreatment with reserpine partially blocked the elevation of plasma glucose and cyclic AMP. The pretreatment with 6-hydroxydopamine or alpha-methyl-p-tyrosine failed to inhibit the increase of plasma glucose and cyclic AMP induced by CPZ. These findings suggest that CPZ acts on the central nervous system and increases plasma glucose and cyclic AMP through epinephrine release from the adrenal medulla. The elevations of plasma glucose and cyclic AMP induced by epinephrine were enhanced by CPZ. CPZ increased plasma glucose and cyclic AMP significantly at high room temperatures (28 and 33 degrees C) at which CPZ did not decrease body temperature. The mechanism of CPZ action is discussed in relation to the increase in the plasma glucose and cyclic AMP levels.

Adrenal Glands↗
PubMed1980

Histochemical staining of cadmium with benzothiazolylazophenol derivatives.

As part of the continuous developmental research for a highly sensitive chelating agent for cadmium, benzothiazolylazophenol derivatives (BTAP) were synthesized and their staining properties for cadmium were examined. The compounds synthesized for this study were identified as being BTAP by analysis of their melting points and C,H,N,S content. Benzothiazolylazo-p-methoxyphenol, -p-chlorophenol and -p-cresol stained cadmium with the highest optical density and the most precise localization amongst dyestuffs reported to date. Differential sequestration by pyrophosphate makes it possible to distinguish cadmium masked by the presence of zinc. With the modification of a chelating agent to increase sensitivity, the improvement in molar absorptivity was also considered theoretically.

Animals↗
PubMed1980

Effects of alpha- and beta-adrenergic blockers on chlorpromazine-induced elevation of plasma glucose and cyclic AMP in fed mice.

The subcutaneous administration of chlorpromazine (CPZ) caused a dose response increase in plasma glucose and cyclic AMP levels in fed male mice. Hexamethonium abolished the elevation of both plasma glucose and cyclic AMP. Propranolol did not inhibit the elevation of plasma glucose but inhibited the increase of plasma cyclic AMP. In contrast, phentolamine and yohimbine completely suppressed the elevation of plasma glucose but not that of plasma cyclic AMP. These results indicate that the hyperglycemia due to CPZ was mediated through the stimulation of alpha-adrenoceptor and on the contrary CPZ increased plasma cyclic AMP through the stimulation of beta-adrenoceptor and that the increase in plasma glucose induced by CPZ was independent of the activation of adenylate cyclase and the increased plasma cyclic AMP. In addition, in contrast to phentolamine and yohimbine, phenoxybenzamine was ineffective to prevent the hyperglycemia induced by CPZ. Moreover, a higher dose of dihydroergotamine was required to inhibit the hyperglycemia.

Adrenergic alpha-Antagonists↗
PubMed1980

Effect of morphine on the release of thyroid-stimulating hormone stimulated by exposure to cold, thyroidectomy and the administration of thyrotrophin releasing hormone in male rats.

Morphine reduced the release of thyroid-stimulating hormone (TSH) which stimulated by exposure to cold and by thyroidectomy as well as reducing the basal level of TSH in the serum of male rats. Thi inhibitory effect of morphine was antagonized by naloxone which did not enhance the basal or cold-induced TSH release. Pretreatment with morphine did not reduce the release of TSH induced by exogenous thyrotrophin-releasing hormone (TRH) but enhanced it. This effect of morphine was also antagonized by naloxone. The above results suggested that the effect of morphine in reducing levels of serum TSH was not mediated by blocking the effect of TRH on the anterior pituitary gland, but that it was probably mediated by the inhibition of the release of TRH.

Animals↗