The Pathophysiology of Rhinitis: II. Assessment of the Sources of Protein in Histamine-induced Nasal Secretions

Raphael, Gordon D.; Meredith, Scott D.; Baraniuk, James N.; Druce, Howard M.; Banks, Steven M.; Kaliner, Michael

doi:10.1164/ajrccm/139.3.791

Cited by 165 publications

(99 citation statements)

References 5 publications

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“…In addition, serous and mucous secretion into the nasal cavity reduce its patency. Both bradykinin and histamine induce this secretion (Baraniuk et al, 1990;Raphael et al, 1989) and differences in their potencies may reflect the inability of L-NAME to attenuate histamine-induced nasal blockage. The patency of the nasal cavity is also reduced by swelling of the nasal mucosa resulting from increased microvascular permeability and increased blood flow.…”

Section: Resultsmentioning

confidence: 99%

Attenuation of human nasal airway responses to bradykinin and histamine by inhibitors of nitric oxide synthase

Dear

Ghali

Foreman

1996

British J Pharmacology

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1 The effects of inhibitors of nitric oxide synthase and local anaesthetics were studied on changes in human nasal airway patency and albumin extravasation in response to bradykinin and histamine, in vivo. 2 Compared with the action of the vasoconstrictor, ephedrine, 2.5 ,umol, N0-nitro-L-arginine methyl ester (L-NAME), 1 pmol alone, did not change the resting value of the minimal cross-sectional area (A min) of the human nasal airway. L-NAME, 0.1 to 10 ymol, produced a dose-related inhibition of the reduction in A min caused by bradykinin, 300 pig. NG-monomethyl-L-arginine (L-NMMA), 1 pimol, similarly reduced the effect of bradykinin, 300 ,ug, on A min, but NG-nitro-D-arginine methyl ester (D-NAME), had no effect. L-NAME, 0.1 to 10 pmol, or L-NMMA, 10 imol, failed to inhibit the effect of histamine, 300 pg on A min. 3 The inhibition by L-NAME, 1 ,umol of the action of bradykinin, 300 pg on A min was maximal between 15 and 30 min after pretreatment with L-NAME.4 L-NAME, 1 and 10 pimol, inhibited the extravasation of albumin into the nasal cavity induced by bradykinin, 300 pug, and also by histamine, 300 pug. D-NAME, 1 and 10 ,umol had no effect on the extravasation of albumin in response to bradykinin or histamine. 5 L-Arginine, 30 pmol, reversed the effect of L-NAME, 1 Mmol, on the bradykinin-and histamineinduced albumin extravasation into the nasal airway. 6 Local anaesthesia of the nasal airway with lignocaine, 10 mg, or benzocaine, 10 mg, failed to inhibit the reduction in A min or the albumin extravasation induced by either bradykinin, 300 mig, and histamine, 300 Mig. 7 We conclude that the extravasation of plasma albumin caused by bradykinin and by histamine involves the generation of nitric oxide. The nasal blockage induced by bradykinin involves nitric oxide generation but the nasal blockage induced by histamine does not.

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Section: Resultsmentioning

confidence: 99%

Attenuation of human nasal airway responses to bradykinin and histamine by inhibitors of nitric oxide synthase

Dear

Ghali

Foreman

1996

British J Pharmacology

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“…Some investigations indicate that histamine caused sneezing and nasal rubbing by its binding to H 1 -receptors on sensory nerve endings. [18][19][20][21] As a matter of course, there are some findings that histamine H 1 -receptor antagonists inhibited the symptoms of sneezing and nasal rubbing of allergic rhinitis model in mice and rats. 22,23) Moreover, other investigators have shown that the suppression of antigen-specific IgE production inhibited the nasal symptoms of an allergic rhinitis model.…”

Section: Discussionmentioning

confidence: 99%

Effects of Lactobacillus acidophilus Strain L-55 on Experimental Allergic Rhinitis in BALB/c Mice

Sunada¹,

Nakamura²,

Kamei

2007

Biological & Pharmaceutical Bulletin

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We investigated the effect of Lactobacillus acidophilus strain L-55 isolated from infant feces on experimental allergic rhinitis in BALB/c mice. The heat-treated cells of strain L-55 were orally administrated for 4 consecutive weeks to mice sensitized by ovalbumin (OVA), and nasal symptoms (sneezing and nasal rubbing) induced by OVA challenge were evaluated. Strain L-55 at doses of 1 and 10 mg cells/mouse significantly inhibited nasal symptoms by repeated administration over a period of 2 weeks. Furthermore, we measured the level of OVA-specific IgE titers in the serum by passive cutaneous anaphylaxis (PCA) reaction. PCA titers in the sera from mice administrated strain L-55 were significantly lowered compared with the control. These results suggest that oral administration of strain L-55 may be useful for alleviating the nasal symptoms of allergic rhinitis.

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“…The sources of human nasal secretions have been previously analyzed by measuring the secretion of albumin (Alb),I secretory IgA (sIgA), nonsecretory IgA, and IgG into induced nasal secretions (1,2).2 It was demonstrated that sIgA is a protein produced locally in the nasal mucosa, processed exclusively by the submucosal glands (1). The secretion of sIgA into nasal secretions is regulated by processes that govern glandular secretion (e.g., the cholinergic nervous system), and therefore sIgA can be used as a marker of glandular secretion.…”

Section: Introductionmentioning

confidence: 99%

Pathophysiology of rhinitis. Lactoferrin and lysozyme in nasal secretions.

Raphael

Jeney²,

Baraniuk³

et al. 1989

J. Clin. Invest.

178

102

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The Pathophysiology of Rhinitis: II. Assessment of the Sources of Protein in Histamine-induced Nasal Secretions

Cited by 165 publications

References 5 publications

Attenuation of human nasal airway responses to bradykinin and histamine by inhibitors of nitric oxide synthase

Attenuation of human nasal airway responses to bradykinin and histamine by inhibitors of nitric oxide synthase

Effects of Lactobacillus acidophilus Strain L-55 on Experimental Allergic Rhinitis in BALB/c Mice

Pathophysiology of rhinitis. Lactoferrin and lysozyme in nasal secretions.

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