Biomedical subjects

K Tasaka

Publications and source records attributed to K Tasaka.

312 records · Page 18Linked to original sources

PubMedDate not supplied

Substance P-induced histamine release from rat peritoneal mast cells and its inhibition by antiallergic agents and calmodulin inhibitors.

Substance P-induced histamine release and Ca2+ release from the intracellular Ca store of rat peritoneal mast cells were inhibited by both antiallergic drugs and microtubule inhibiting agents. It was found that in the case of antiallergic compounds, histamine release inhibition may be intimately related to the inhibition of Ca2+ release from the intracellular store in which the microtubules play an important role. When mast cells were pretreated with either theophylline or dibutyryl cAMP, the inhibition of histamine release was closely related to the inhibition of Ca2+ release from the intracellular Ca store. Calmodulin inhibitors were also effective in inhibiting histamine release from mast cells induced by substance P. The inhibitory potencies of calmodulin inhibitors on histamine release from mast cells were closely correlated with those exerted on calmodulin activity.

Animals↗

PubMedDate not supplied

Identification of vimentin in rat peritoneal mast cells and its phosphorylation in association with histamine release.

Stimulation of rat peritoneal mast cells with histamine releasers, such as compound 48/80 and substance P, caused a similar pattern of protein phosphorylations: the molecular weights of the two major phosphorylated proteins were 45 kDa and 59 kDa. When rat mast cells permeabilized with beta-escin were exposed to Ca2+ at concentrations higher than 0.6 microM, phosphorylated proteins of identical molecular weight were also detected. By a radioimmunoprecipitation assay using anti-vimentin mouse monoclonal antibody, the 59 kDa protein was identified as vimentin, one of the intermediate cytoskeletal proteins. Moreover, it became apparent that the phosphoamino acid in phosphorylated vimentin was a serine residue. Sequential changes in vimentin phosphorylation were similar to that of histamine release elicited by histamine releasers: phosphorylation took place within 5 s of stimulation and reached a maximum within 10 s. When permeabilized mast cells were treated with calphostin C, a specific protein kinase C inhibitor, phosphorylation was markedly inhibited. Fluorescence images of mast cells stained with FITC-labelled anti-vimentin antibody showed filamentous structures surrounding the granules in the cytoplasm. However, after exposure to compound 48/80, the filamentous structures promptly disappeared and a dim fluorescence was observed homogeneously in the cell indicating that a rapid depolymerization of vimentin had taken place. From the present study, it became clear that when rat peritoneal mast cells were stimulated, vimentin was rapidly phosphorylated by protein kinase C and this phosphorylation process seems to be related to histamine release.

Animals↗

PubMedDate not supplied

Effects of thyrotropin-releasing hormone and phorbol ester on dopamine release from dispersed rat tuberoinfundibular dopaminergic neurons.

We have investigated the intracellular mechanisms underlying thyrotropin-releasing hormone (TRH)-mediated [3H]dopamine ([3H]DA) release from dispersed rat tuberoinfundibular dopaminergic (TIDA) neurons. The specific binding of [3H]Me-TRH to these cells is characterized by a single, high-affinity binding site (Kd = 1.2 nM) with a Bmax value of 178 fmol/mg protein. Thyrotropin-releasing hormone markedly increased [3H]DA release and intracellular free calcium concentration ([Ca2+]i) in TIDA neurons, and its effect was abolished by treatment with EGTA (5 mM) or chlordiazepoxide, a specific TRH receptor antagonist (10 microM). Furthermore, to examine the involvement of protein kinase C on [3H]DA release, we investigated the effect of phorbol myristate acetate (PMA), which is known to activate protein kinase C directly. Phorbol myristate acetate induced a significant increase in [3H]DA release in a concentration-dependent manner. Treatment with TRH (1 microM) plus PMA (100 nM) resulted in an additive increase in [3H]DA release. Thyrotropin-releasing hormone (1 microM) still increased [3H]DA release even after preincubation with PMA (500 nM) for 24 h, but PMA (100 nM) did not under the same conditions. These results suggest that TRH may induce DA release in dispersed rat TIDA cells by increasing calcium influx and activating the protein kinase C system.

Animals↗

PubMedDate not supplied

A case of undifferentiated carcinoma of the gallbladder with anomalous arrangement of the pancreaticobiliary ductal system.

Anomalous junction of the pancreaticobiliary duct (AJPBD) is a congenital anomaly associated with gallbladder carcinoma. Especially patients with noncystic dilatation and without dilatation of the biliary tract are at risk of gallbladder carcinoma. A 56-year-old woman with advanced gallbladder cancer associated with AJPBD but without dilatation of the biliary tract was treated at our hospital. Although histologically cancer cells remained in the layer of the proprial mucosa, extensive metastases to lymph nodes including the paraaorta and peripancreas were detected. According to the TNM classification this case was of Stage IVB. The cancer consisted of medullary round cells, and was diagnosed as undifferentiated carcinoma. After surgery poor prognosis was expected, but three years have elapsed with no recurrence. The case is of interest because of two points of discrepancy: the primary cancer did not show deep invasion but demonstrated extensive lymph node metastases; the cancer was histologically malignant but prognosis was relatively good.

Bile Ducts↗

PubMedDate not supplied

Comparative study of the adverse effects of various radiographic contrast media, including ioversol, a new low-osmolarity medium. I. Histamine release.

Histamine release induced by some radiographic contrast media (RCM) such as iohexol, iopamidol and meglumine sodium amidotrizoate (MSA) was studied in comparison with ioversol, a new low-osmolarity contrast medium. Although all of the RCM caused a dose-related histamine release from rat peritoneal mast cells, that induced by ioversol was the least. MSA induced more remarkable histamine release than did sodium chloride at each of the corresponding osmolarities, except under hypoosmolar conditions. Moreover, in guinea pig lung perfusion, RCM, especially ioversol, iohexal and iopamidol, induced only a weak histamine release in both non-sensitized and sensitized animals. However, when MSA was perfused in sensitized animals, a large amount of histamine was detected in the lung effluents. These results suggest that nonionic RCM, including ioversol, can be used more safely than MSA for diagnostic examination.

Animals↗

PubMedDate not supplied

Role of hypothalamic histamine in stimulating the corticosterone release in rats.

Intracerebroventricular injection of alpha-fluoromethylhistidine caused a significant decrease of the histamine content of the hypothalamus as well as of plasma adrenocorticotropic hormone and corticosterone concentrations. A high correlation was observed between the histamine content of the hypothalamus and the plasma corticosterone concentration. When the histamine content of the hypothalamus decreased, the plasma concentration of corticosterone diminished. Almost the same result was obtained when the posterior hypothalamus was lesioned electrically. The increases in plasma adrenocorticotropic hormone and corticosterone concentrations, induced by intracerebroventricular injection of histamine in sham-operated rats, were abolished after hypothalamic lesioning. When electrical stimulations were applied to the posterior hypothalamus, plasma adrenocorticotropic hormone and corticosterone concentrations increased significantly and, at the same time, evoked potentials were recorded on the adrenal nerve. An increase in plasma corticosterone concentration, induced by hypothalamic stimulation, was also observed even after hypophysectomy, suggesting that another corticosterone-secreting pathway exists apart from the hypophysis-adrenocortex system. The increase in plasma adrenocorticotropic hormone and corticosterone concentrations was inhibited not only by pyrilamine and cimetidine, but also by (R)-alpha-methyl-histamine, and H3 agonist. In addition, the effect of this latter product was inhibited by thioperamide, an H3 antagonist. These results indicate that hypothalamic histamine plays an important role in the stimulation of the corticosterone release in rats.

Adrenal Glands↗