I Yamawaki

Tokyo Women's Medical University, Edo, Tōkyō, Japan

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Publications (38)126.08 Total impact

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    ABSTRACT: To determine whether adenosine A3 receptor stimulation produces airway inflammation and, if so, what the mechanism of action is, we studied microvascular permeability in the rat trachea. After intravenous injection of Evans blue dye, adenosine and various adenosine analogues were given by inhalation, and the tracheal microvascular permeability was determined by a photometric measurement of extravasated dye. N6-2-(4-aminophenyl)-ethyladenosine (APNEA), an adenosine A3 receptor agonist, dose dependently increased plasma protein extravasation, whereas adenosine, the A1-receptor agonist N6-(R-phenylisopropyl)-adenosine, or the A2-receptor agonist 5'-N-ethyl-carboxamidoadenosine had no effect. The effect of APNEA was not altered by the adenosine A1/A2 receptor antagonist 8-(p-sulphophenyl)-theophylline, but was reduced by depletion of mast cell-derived mediators with compound 48/80 or pretreatment with the tachykinin NK1 receptor antagonist CP99,994. These results suggest that activation of A3 receptor specifically increase airway microvascular permeability probably via mast cell-derived mediators and tachykinins.
    Research communications in molecular pathology and pharmacology 01/2000; 108(1-2):96-107.
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    ABSTRACT: Inhalation of adenosine causes bronchoconstriction in asthmatic subjects, but the effect of this purine nucleotide on airway vascular permeability is unknown. In order to determine whether adenosine produces airway microvascular leakage and, if so, to examine the effect of cromolyn (sodium cromoglycate (SCG)) on this extravasation of Evans blue was measured in the airways of ovalbumin-sensitized Brown Norway rats. Inhaled adenosine caused microvascular leakage in sensitized but not in non-sensitized rats, and the response was abolished by capsaicin pretreatment or the tachykinin neurokinin-1 receptor antagonist FK888. Adenosine-induced vascular leakage became apparent in nonsensitized rats when treated with phosphoramidon, and airway neutral endopeptidase activity was lower in sensitized than in non-sensitized animals. The extravasation induced by adenosine in sensitized rats was dose dependently inhibited by SCG aerosols, SCG likewise inhibited microvascular responses to substance P, but had no effect on those to platelet-activating factor. These results suggest that: 1) adenosine induces airway microvascular leakage in sensitized rats through stimulation of neurokinin-1 receptors; 2) this effect is associated with a sensitization-induced decrease in neutral endopeptidase activity; and 3) sodium cromoglycate inhibits adenosine-induced extravasation, presumably via functional antagonism of tachykinins.
    European Respiratory Journal 12/1999; 14(5):1082-7. · 6.36 Impact Factor
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    ABSTRACT: To determine the effect of the antiallergic drug azelastine on airway mucosal inflammation, we studied airway microvascular permeability in response to platelet-activating factor (PAF) in pathogen-free rats. Vascular permeability and neutrophil accumulation were assessed by the percent area occupied by Monastral blue-labeled blood vessels and by myeloperoxidase-containing granulocytes, respectively, in whole mounts of the trachea and main bronchus. Intravenous PAF caused dose-dependent increases in the area density of Monastral blue-labeled vessels and neutrophil influx, and the former effect was inhibited by depletion of circulating neutrophils by cyclophosphamide or treatment with the neutrophil elastase inhibitor ONO-5046. Pretreatment with azelastine inhibited PAF-induced vascular leakage without affecting neutrophil accumulation. This inhibitory effect of azelastine was not seen in neutropenic rats and ONO-5046-treated rats. PAF increased neutrophil elastase contents in bronchoalveolar lavage fluid, an effect that was inhibited by azelastine. Therefore, azelastine attenuates PAF-induced airway mucosal microvascular leakage, probably involving inhibition of the release of neutrophil elastase from activated neutrophils.
    The American journal of physiology 03/1999; 276(2 Pt 1):L351-7. · 3.28 Impact Factor
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    ABSTRACT: Heparin and related proteoglycans are released from mast cells and possess anti-inflammatory and anti-complement activities. To elucidate whether heparin affects goblet cell secretion in asthmatic airways and, if so, what the mechanism of action is, we studied guinea pigs sensitized with ovalbumin (OVA) by determining the mucus score (MS) of tracheal goblet cells stained with Alcian blue and PAS. Inhalation of OVA caused a rapid decrease in MS in a dose-dependent manner, with the maximal decrease being from 545 +/- 26 to 192 +/- 35 (p < 0.001), indicating an increase in goblet cell mucus discharge. This effect was selectively inhibited by the histamine H2 receptor blockade with cimetidine. Prior inhalation of heparin inhibited OVA-induced goblet cell secretion in a dose-dependent fashion, but had no effect on histamine-induced goblet cell secretion. The OVA-induced histamine release from the tracheal tissue was likewise inhibited by heparin. These results suggest that allergic challenge stimulates airway goblet cell secretion mainly through the release of histamine and the concomitant activation of histamine H2 receptors on goblet cells, and that heparin protects against this effect by inhibiting the histamine release from mast cells.
    Nihon Kokyūki Gakkai zasshi = the journal of the Japanese Respiratory Society. 10/1998; 36(10):845-50.
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    ABSTRACT: To determine whether airway epithelium releases arginine vasopressin (AVP) and, if so, what the mechanism of the release is, we studied cultured human bronchial epithelial cell line, 16-HBE cells, in vitro. The cells spontaneously released small but significant amounts of AVP, and this release was dose dependently increased by platelet-activating factor (PAF) or bradykinin (BK). The PAF- and BK-induced AVP release was inhibited by 2-nitro-4-carboxyphenyl-N,N-diphenylcarbamate, a phospholipase C inhibitor, and thapsigargin but not by Ca2+-free solution. Pretreatment with the big conductance Ca2+-activated K+ channel blocker iberiotoxin attenuated the stimulated release of AVP, whereas apamin and glibenclamide were without effect. These results suggest that human bronchial epithelial cells release AVP and that the release may be stimulated by phospholipase C activation, mobilization of Ca2+ from internal stores and the concomitant activation of big conductance Ca2+-activated K+ channels.
    Regulatory Peptides 07/1998; · 2.06 Impact Factor
  • I Yamawaki, J Tamaoki, Y Takeda, A Nagai
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    ABSTRACT: We examined the effects of adenosine and its analogues on vascular permeability in rat trachea using Evans blue dye as a marker for plasma leakage. Inhalation of N6-2-(4-aminophenyl) ethyladenosine (APNEA), a specific A 3 receptor agonist, increased microvascular leakage in a dose-dependent manner, but adenosine, [R]-N6-(1-Methyl-2-phenylethyl) adenosine (R-PIA), aspecific A 1 receptor agonist, and 5'-(N-ethyl-carboxamide) adenosine (NECA), a specific A 2 receptor agonist, had no effect. Inhalation of capsaicin increased vascular permeability in a dose-dependent manner. Pretreatment with NECA (10-1000 nmol/kg, i.v.) but not adenosine (100 nmol/kg i.v.), R-PIA (100 nmol/kg, i.v.) or APNEA (100 nmol/kg, i.v.) inhibited microvascular leakage produced by capsaicin aerosol (3 x 10(-5) M) in a dose-dependent manner. However, NECA (10-100 nmol/kg, i.v.) failed to inhibit substance P aerosol (10(-4) M)-induced extravasation of the dye. These findings suggest that stimulation of adenosine A 3 receptors produces airway vascular permeability, and that A 2 receptors inhibit neurogenic plasma extravasation, presumably by inhibiting the release of tachykinins from sensory nerves.
    Nihon Kokyūki Gakkai zasshi = the journal of the Japanese Respiratory Society. 04/1998; 36(3):231-5.
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    ABSTRACT: A case of pulmonary eosinophilic granuloma that underwent spontaneous remission is presented. A 23-year old man presented with dry cough and fever. Chest X-ray film revealed diffuse reticulo-nodular infiltrates in the middle and upper lung fields. Chest CT and HRCT showed multiple cystic lesions with thick walls and small nodules predominantly in the inner zone. Based on radiographic findings, pulmonary eosinophilic granuloma was suspected. Bronchoalveolar lavage cell data showed lymphocyte and eosinophil alveolitis with no increase of CD 1 lymphocytes. The symptoms and radiographic findings improved markedly within 4 months after the onset of symptoms without treatment and upon cessation of smoking. Chest CT and HRCT showed that the cystic walls were thinner and that the small nodules had decreased. Thoracoscopic lung biopsy revealed granulomatous lesions consisting of CD 1 and S-100 protein positive histiocytes with infiltration of eosinophils and fibrous lesions. Pulmonary eosinophilic granuloma was diagnosed. There has been no recurrence for 1 year.
    Nihon Kokyūki Gakkai zasshi = the journal of the Japanese Respiratory Society. 02/1998; 36(1):90-4.
  • I Yamawaki, J Tamaoki, Y Takeda, A Nagai
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    ABSTRACT: To determine whether sodium cromoglycate (SCG) inhibits airway neurogenic inflammation and, if so, to elucidate the mechanism of its action, we studied plasma extravasation evoked by hypertonic saline in the rat trachea by measuring the amount of extravasated Evans blue dye. Inhalation of hypertonic saline (5-15% NaCl) produced microvascular leakage, an effect that was reduced by pretreatment with SCG in a dose-dependent manner. Inhaled SCG (10 mg/ml) for 2 min did not affect the basal vascular permeability, but significantly inhibited the 10% NaCl-induced plasma extravasation by 34%. SCG likewise inhibited the responses of microvascular leakage to substance P aerosols, whereas it was without effect on those to platelet activating factor aerosols. These results suggest that SCG inhibits airway neurogenic inflammation presumably via functional antagonism of tachykinins, and that this novel effect may be involved in the therapeutic efficacy of SCG in the treatment of airway inflammatory diseases including asthma.
    Research communications in molecular pathology and pharmacology 01/1998; 98(3):265-72.
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    ABSTRACT: A 64-year-old woman with a history of old tuberculosis, had a fungus ball shadow with meniscus sign in the upper right lung field on a chest X-ray film in 1991. Based on the chest X-ray findings, pulmonary aspergilloma was suspected. Because the size of the intracavitary fungus ball increased, the patient was treated with itraconazole over one year in 1995, but there was no improvement. One month later, she was admitted because of fever, hemoptysis and productive cough, and chest X-ray showed an enlargement of intracavitary mass and infiltrative shadow in the right lung. Chronic necrotizing aspergillosis was diagnosed on the basis of her clinical and radiographic features, and positive serological test. Although itraconazol and amphotericin B were given, cavity and intracavitary fungus ball shadow kept growing. Combination therapy of antifungal drugs and ulinastatin markedly improved symptoms and resulted in complete disappearance of the fungus ball on chest CT scan.
    Nihon Kyōbu Shikkan Gakkai zasshi 10/1997; 35(9):991-5.
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    ABSTRACT: To determine the role of neutrophil elastase in allergen-induced airway microvascular leakage, we assessed vascular permeability of guinea pig trachea by measuring the extravasation of Evans blue dye in the circulating blood. Inhalation of ovalbumin (OA) to guinea pigs sensitized with OA caused Evans blue extravasation, indicating an increased microvascular permeability. Pretreatment with ONO-5046 a specific inhibitor of neutrophil elastase, inhibited OA-induced vascular leakage in a dose-dependent manner. Tracheal instillation of human neutrophil elastase likewise increased microvascular permeability, and this effect was almost completely abolished by ONO-5046. Challenge with OA increased the number of neutrophils and neutrophil elastase activity in the bronchoalveolar lavage fluid, and these effects were inhibited by ONO-5046. These results suggest that neutrophil accumulation into the airway and the subsequent release of neutrophil elastase may play a role in the airway microvascular leakage produced by antigen challenge.
    Arerugī = [Allergy] 07/1997; 46(6):496-501.
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    ABSTRACT: We encountered six patients with pneumonitis related to blended chinese traditional medicine (Kampo). The duration of treatment with kampo ranged from 14 to 110 days (mean: 38 days). The most common complaints were dyspnea, fever, and dry coughing. Fine crackles were heard at the bases of both lungs. Abnormal laboratory findings included high values of C-reactive protein and glutamic-oxaloacetic transaminase in all patients, lactate dehydrogenase in 5 patients, and eosinophil count in 1 patient. Chest X-ray films and CT films revealed diffuse reticulo-nodular interstitial shadows with consolidation in both lung fields in 3 patients and pleural effusion in 1 patient. Bronchoalveolar lavage was done in 4 patients; examination of the lavage fluid showed lymphocyte alveolitis, either pure or associated with neutrophilia and eosinophilia in 3 patients. Inverted CD4/CD8 lymphocyte ratios were found in 3 patients. Transbronchial lung biopsy was done in 4 patients and specimens from 3 of those 4 showed organizing pneumonitis with thickening of alveolar septa. Lymphocyte stimulation tests were positive in 4 patients. Discontinuation of the drug (2 patients) or administration of corticosteroids (4 patients) was followed by rapid improvement. Patients being treated with kampo preparations should be observed for signs and symptoms of drug-induced pneumonitis.
    Nihon Kyōbu Shikkan Gakkai zasshi 01/1997; 34(12):1331-6.
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    ABSTRACT: We studied the effects of macrolides on lipopolysaccharide (LPS)-induced airway goblet cell secretion in the guinea pig trachea. The goblet cell secretion was assessed in histological sections of the tracheal mucosa stained with alcian blue and periodic acid Schiff by arbitrarily determining mucus score, which is inversely related to the magnitude of mucus discharge. Inhalation of Escherichia coli LPS (5 mg/kg) caused a time-dependent decrease in mucus score, with the maximal response being from 542 +/- 49 to 92 +/- 20 arbitrary units (P < 0.001) after 3 h, which was accompanied by an increase in the number of neutrophils in the tracheal mucosa. The LPS-induced mucus discharge was inhibited by oral clarithromycin and erythromycin in a dose-dependent manner (5 and 10 mg/kg), whereas amoxicillin and cefaclor had no effect. Each dose of clarithromycin and erythromycin, but not amoxicillin or cefaclor, likewise attenuated the LPS-induced recruitment of neutrophils. These results suggest that LPS stimulates goblet cell secretion and neutrophil accumulation in the airways and that macrolides may be of value in protecting against neutrophil-associated airway hypersecretion.
    The American journal of physiology 01/1997; 272(1 Pt 1):L15-9. · 3.28 Impact Factor
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    ABSTRACT: A 75-year-old woman had an irregularly shaped cavitary lesion in the right upper lung field on a chest X-ray film and a CT scan. Primary lung cancer was suspected, but no evidence of malignancy or of infection was found on examination of specimens obtained by transbronchial biopsy and by lavage. Seven months after the first examination the cavity was found to have enlarged and an intra-cavitary fungus ball like shadow was seen. On the basis of these findings, pulmonary aspergilloma with or without primary lung cancer was suspected. Examination of a specimen obtained by transbronchial biopsy revealed squamous cell carcinoma. Right upper lobectomy was done, and the resected tissue included a polypoid nodule and a cavity wall composed of a milky-white solid tumor. Microscopic examination revealed a moderately differentiated squamous cell carcinoma in both the cavity wall and the polypoid nodule, and no evidence of fungal involvement.
    Nihon Kyōbu Shikkan Gakkai zasshi 12/1996; 34(11):1289-93.
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    ABSTRACT: A 72-year-old man was being treated with Saiboku-to for throat discomfort. Forty-two days after the start of Saiboku-to therapy, dyspnea and fever developed and he was admitted to the hospital. Arterial blood gas analysis showed arterial hypoxemia, and a chest X-ray film and chest CT scan showed diffuse linear-nodular shadows in both lung fields. The results of a lymphocyte-stimulation test were positive for Saiboku-to and Saiboko-to-induced pneumonia was diagnosed. Saiboku-to was stopped and prednisolone was given. The symptoms, respiratory status and chest X-ray findings markedly improved. To our knowledge, this is the fifth case of Saiboku-to-induced pneumonia reported in Japan.
    Nihon Kyōbu Shikkan Gakkai zasshi 12/1996; 34(11):1239-43.
  • I Yamawaki, J Tamaoki, Y Takeda, K Konno
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    ABSTRACT: The action of the anti-asthmatic drug sodium cromoglycate (SCG) on airway inflammation remains uncertain. Using Evans blue dye as a maker of plasma leakage, we studied the effect of SCG on neurogenic vascular extravasation evoked by hypertonic saline (HTS) in the rat trachea. Inhalation of HTS (5-15%) caused a concentration-dependent increase in plasma leakage, but inhaled 0.9% NaCl had no effect. Inhalation of SCG did not affect the baseline level of vascular permeability, but it inhibited the effect of HTS in a dose-dependent manner: plasma extravasation induced by 10% NaCl was significantly reduced by 2 minutes of inhalation of SCG at concentrations of 10 and 50 mg/ml (p < 0.05 and p < 0.01, respectively). SCG (10 mg/ml), also inhibited the changes in microvascular permeability caused by aerosols of substance P (10(-4) M), whereas it did not affect the responses to aerosols of platelet-activating factor (3 x 10(-4) M). A similar dose of SCG did not significantly alter microvascular leakage caused by 5% NaCl. However, phosphoramidon, a selective inhibitor of neutral endopeptidase, potentiated the response to 5% NaCl, an effect that was inhibited by SCG (p < 0.05). These results suggest that SCG inhibits HTS-induced airway vascular permeability, presumably through a tachykinin-antagonist-like property, and that this inhibition is exaggerated when the activity of endogenous neutral endopeptidase is low.
    Nihon Kyōbu Shikkan Gakkai zasshi 09/1996; 34(9):973-7.
  • J Tamaoki, E Tagaya, I Yamawaki, K Konno
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    ABSTRACT: To elucidate the effect of hypoxia on nitrovasodilator-induced pulmonary vasodilation, we studied canine pulmonary arterial rings under isometric conditions in vitro. Exposure to hypoxia inhibited the relaxant responses of KCl-contracted tissues to sodium nitroprusside (SNP), so that the maximal relaxation (Emax) and the negative logarithm of molar concentration required to produce 50% relaxation (pD2) were decreased from 92 +/- 7 to 62 +/- 5% and from 5.8 +/- 0.2 to 4.7 +/- 0.3, respectively (means +/- SE, P < 0.01 for each). This effect was likewise observed when 8-bromoguanosine-3',5'-cyclic monophosphate was used as a relaxant. The impairment of SNP-induced relaxation of endothelium-denuded rings under hypoxia was abolished by ouabain or K(+)-free solution. Incubation with SNPincreased intracellular cGMP contents in a dose dependent manner, an effect that was not altered by hypoxia. SNP also increased ouabain-sensitive 86Rb uptake, and this effect was inhibited by hypoxia. These results suggest that hypoxia reduces nitrovasodilator-induced relaxation of pulmonary artery, probably through an inhibition of cGMP-dependent sarcolemmal Na-K-adenosine triphosphatase activity.
    The American journal of physiology 08/1996; 271(1 Pt 1):L172-7. · 3.28 Impact Factor
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    ABSTRACT: We studied the effect of T-kinin on airway vascular permeability and its modulation by endogenous peptidases in anesthetized rats in vivo, Vascular permeability was assessed by photometric measurement of extravasated Evans blue dye after formamide extraction. Intravenous injection of T-kinin increased dye extravasation in the trachea and main bronchi in a dose-dependent manner. Plasma extravasation evoked by T-kinin was inhibited by Hoe 140, a B2 receptor but-not by des Arg9-Leu8-bradykinin, a B1 receptor antagonist. Treatment with captopril, an angiotensin-converting enzyme inhibitor, potentiated the T-kinin-induced plasma extravasation, whereas phosphoramidon, a neutral endopeptidase inhibitor, had no effect. These results suggest that T-kinin increases airway vascular permeability via stimulation of B2 receptors, and that this effect is modulated by endogenous angiotensin-converting enzyme.
    Nihon Kyōbu Shikkan Gakkai zasshi 07/1996; 34(6):627-31.
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    ABSTRACT: The effect of lipoxin A4 and lipoxin B4 on cholinergic neurotransmission in rabbit tracheal segments was studied under isometric conditions in vitro. Lipoxin A4 attenuated the contractile responses to electrical field stimulation and caused a rightward shift of the frequency-response curves, so that the stimulus frequency required to produce a half-maximal effect (ES50) increased from 8.1 +/- 0.8 to 25.7 +/- 1.9 Hz (P < 0.001), whereas lipoxin B4 had no effect. In contrast, lipoxin A4 did not alter the contractile responses to acetylcholine. Pretreatment of tissues with NG-nitro-L-arginine methylester inhibited the effect of lipoxin A4 on electrical field stimulation, but NG-nitro-D-arginine methylester did not. This inhibition by NG-nitro-L-arginine methylester was reversed by L-arginine but not by D-arginine. These results suggest that lipoxin A4 prejunctionally reduces the vagal nerve-mediated contraction of airway smooth muscle, probably by inhibiting the release of acetylcholine, and that this effect may be exerted through stimulation of nitric oxide generation.
    European Journal of Pharmacology 12/1995; 287(3):233-8. · 2.59 Impact Factor
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    ABSTRACT: T-kinin (Ile-Ser-bradykinin), the product of T-kininogen, has been found in rat plasma during systemic inflammation, but the effect of this kinin on airway inflammatory response is unknown. We examined the effect of T-kinin on vascular permeability in airways of anesthetized rats in vivo by using photometric measurement of the extravasated Evans blue. Intravenous injection of T-kinin (0.1-10 mumol/kg) increased dye extravasation in a dose-dependent manner, with 134% for trachea and 117% for bronchi by 1 mumol/kg. Pretreatment with bradykinin B2-receptor antagonist Hoe-140 (100 nmol/kg), but not the B1-receptor antagonist des-Arg9-Leu8-bradykinin (5 mg/kg), abolished plasma extravasation evoked by T-kinin (1 mumol/kg). NK1 tachykinin-receptor antagonist CP-99994 (4 mg/kg) did not affect T-kinin-induced vascular leakage. Pretreatment with captopril (2.5 mg/kg), angiotensin-converting enzyme inhibitor, potentiated T-kinin (100 nmol/kg)-induced plasma extravasation, whereas phosphoramidon (2.5 mg/kg), a neutral endopeptidase inhibitor, had no effect. We conclude that T-kinin produces airway vascular extravasation via stimulation of B2 receptors. The effect is modulated by endogenous angiotensin-converting enzyme and is not mediated via activation of sensory nerve.
    Journal of Applied Physiology 11/1995; 79(4):1129-33. · 3.48 Impact Factor
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    ABSTRACT: Nitric oxide (NO) may play a part in pulmonary vascular regulation and bronchomotor control and has been detected in exhaled air. We report the release of NO from airway epithelial cells and its regulation by cyclic adenosine monophosphate (cAMP). To directly measure NO release, a highly specific amperometric sensor for NO made of Pt/Ir alloy coated with a three-layered membrane consisting of KCI, NO-selective resin, and normal silicon resin was developed. Immersion of this sensor in the medium containing canine cultured tracheal epithelium detected baseline levels of NO at 9.6 +/- 1.6 nM (mean +/- SE), which was reduced by NG-nitro-L-arginine methylester (L-NAME) but not by D-NAME. This inhibition was reversed by L-arginine. Addition of isoproterenol, 3-isobutyl-1-methylxanthine, and forskolin caused a rapid increase in NO, an effect that was not altered by Ca(2+)-free medium in the presence of the intracellular Ca2+ chelator BAPTA-AM and the calmodulin antagonist W-7. Bradykinin, ionomycin, and ATP were without effect on NO release. The forskolin-induced NO release was accompanied by intracellular accumulation of cAMP and Ca2+. In contrast, bradykinin increased intracellular Ca2+ but not cAMP levels. Cytochemistry of cultured tracheal epithelium showed a positive staining with NADPH diaphorase activity. These results suggest that airway epithelial cells spontaneously release NO and that the release may be stimulated specifically through cAMP-dependent mechanism.
    American Journal of Respiratory and Critical Care Medicine 11/1995; 152(4 Pt 1):1325-30. · 11.04 Impact Factor