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Biomedical subjects

S Mue

Publications and source records attributed to S Mue.

97 records · Page 6Linked to original sources
PubMedDate not supplied

Suppression by adrenoceptor beta-agonists of vascular permeability increase and edema formation induced by arachidonate metabolites, platelet-activating factor, and tumor-promoting phorbol ester TPA.

Air-pouch-type inflammation was induced by injecting sodium carboxymethyl cellulose solution containing leukotriene C4 (LTC4, 3.20 x 10(-7) M, 0.2 micrograms/ml) and prostaglandin E2 (PGE2, 5.68 x 10(-6) M, 2.0 micrograms/ml), platelet-activating factor (PAF, 1 x 10(-6) M, 0.52 micrograms/ml), or 12-O-tetradecanoyl phorbol 13-acetate (TPA, 1.62 x 10(-6) M, 1.0 micrograms/ml) into an air pouch made on the dorsum of rats. Vascular permeability and tissue edema formation were significantly increased by injecting the phlogogen solution. The histamine level in the pouch fluid was dramatically increased by injecting TPA but not by LTC4 and PGE2, or PAF. Injection of isoproterenol or procaterol with the phlogogen solution produced dose-dependent suppression of both vascular permeability increase and tissue edema formation. However, the TPA-induced increase in the histamine level was not suppressed in parallel with the decrease of vascular permeability or tissue edema formation. These results indicate that beta-agonists suppress vascular permeability response and local tissue edema formation not by inhibiting mast cell degranulation, but by inhibiting the reactivity of the local vasculature to chemical mediators such as arachidonate metabolites, PAF, and histamine and serotonin released from mast cells.

Adrenergic beta-Agonists↗
PubMedDate not supplied

Role of phosphatidylinositol 3-kinase in degranulation induced by IgE-dependent and -independent mechanisms in rat basophilic RBL-2H3 (ml) cells.

We have examined the role of phosphatidylinositol 3-kinase (P13-kinase) in the degranulation induced by the antigen, an IgE-dependent stimulant, and by carbachol and thapsigargin, IgE-independent stimulants, in the muscarine ml receptor-transfected mast cell line RBL-2h3 (ml) cells. These stimulants commonly increased P13-kinase activity in the anti-phosphotyrosine immunoprecipitate. The P13-kinase inhibitors wortmannin and LY294002 inhibited induced by these stimulants. The membrane ruffling induced by the antigen or carbachol was also inhibited by wortmannin. In contrast, thapsigargin induced by membrane ruffling but induced microspikes, which was not affected by wortmannin. In the permeabilized RBL-2H3 (ml) cells, wortmannin the GTP gamma S-induced membrane ruffling without inhibiting the GTP gamma S-induced degranulation. These findings suggest that P13-kinase is involved not only in IgE-dependent degranulation but also in IgE-independent degranulation, and that the GTP gamma S-sensitive protein at the downstream of P13-kinase is responsible for the degranulation but not for the membrane ruffling.

Androstadienes↗
PubMedDate not supplied

Negative regulation of MAP kinase by diacylglycerol-dependent mechanisms via G protein-coupled receptors in rat basophilic RBL-2H3 (ml) cells.

Carbachol and 5'-(N-ethylcarboxamido)-adenosine (NECA), stimulants of G protein-coupled receptors, induce MAP kinase activation in the muscarinic ml receptor-transfected mast cell line, RBL-2H3 (ml) cells. The phospholipase C inhibitor neomycin and the phosphatidate phosphohydrolase inhibitor propranolol augmented MAP kinase activation induced by carbachol and NECA without affecting the antigen-induced MAP kinase activation. Furthermore, the duration of MAP kinase activation induced by carbachol or NECA was also prolonged by neomycin and propranolol. The specific protein kinase C inhibitor Ro 31-8425 enhanced the carbachol- or NECA-induced MAP kinase activation. These findings suggest that the MAP kinase activation mediated by the G protein-coupled receptors is negatively regulated by diacylglycerol and activated protein kinase C(s).

Adenosine↗
PubMedDate not supplied

Bronchial responses to enalapril in asthmatic, hypertensive patients.

The subjects, six asthmatic patients with mild essential hypertension, were aged 48 to 63 years and each was being treated with theophylline. Five patients received 10 mg of enalapril daily for two weeks and one received 5 mg for four weeks. Their bronchial responses to inhaled methacholine were measured with a modification of the 3-Hz oscillation method before and after the enalapril treatment. The patients' mean blood pressures decreased significantly from 180.7/100.3 to 152.0/93.3 mmHg after treatment. No treatment-associated changes in the frequency of coughing, the number of asthmatic attacks, or use of antiasthmatic drugs were noted. The results of the bronchial provocation tests revealed no changes in bronchial sensitivity or reactivity during treatment. Serum substance P levels were 61.3 pg/ml before treatment and 60.2 pg/ml after treatment. It is concluded that therapeutic doses of enalapril did not exacerbate asthmatic attacks or increase bronchial hypersensitivity in these asthmatic, hypertensive patients.

Asthma↗