Ovalbumin increases macromolecular efflux from the in situ nasal mucosa of allergic hamsters

1998 ◽  
Vol 84 (1) ◽  
pp. 169-176 ◽  
Author(s):  
Xiao-Pei Gao ◽  
Syed R. Akhter ◽  
Israel Rubinstein
Keyword(s):  
Nitric Oxide ◽  
Methyl Ester ◽  
Nasal Mucosa ◽  
Biosynthetic Pathway ◽  
Fluorescein Isothiocyanate ◽  
Significant Time ◽  
Hoe 140 ◽  
Subsequent Activation

Gao, Xiao-Pei, Syed R. Akhter, and Israel Rubinstein.Ovalbumin increases macromolecular efflux from the in situ nasal mucosa of allergic hamsters. J. Appl. Physiol. 84(1): 169–176, 1998.—The purpose of this study was to determine whether bradykinin mediates ovalbumin-induced increase in macromolecular efflux from the nasal mucosa of ovalbumin-sensitized hamsters in vivo and, if so, whether thel-arginine/nitric oxide biosynthetic pathway transduces, in part, this response. We found that suffusion of ovalbumin onto the in situ nasal mucosa of ovalbumin-sensitized hamsters, but not of controls, elicited a significant time- and concentration-dependent increase in clearance of fluorescein isothiocyanate-labeled dextran (mol mass, 70 kDa; P < 0.05). HOE-140, but not des-Arg9,[Leu8]-bradykinin, and N G-l-arginine methyl ester (l-NAME), but not N G-d-arginine methyl ester, significantly attenuated ovalbumin-induced responses.l-Arginine, but notd-arginine, abolished the effects ofl-NAME.l-NAME also significantly attenuated bradykinin-, but not adenosine- induced increase in macromolecular efflux from the in situ nasal mucosa. Overall, these data suggest that ovalbumin increases macromolecular efflux from the in situ nasal mucosa of ovalbumin-sensitized hamsters, in part, by producing bradykinin with subsequent activation of thel-arginine/nitric oxide biosynthetic pathway.

scholarly journals Methotrexate potentiates bradykinin-induced increase in macromolecular efflux from the hamster oral mucosa

1997 ◽  
Vol 273 (4) ◽  
pp. R1254-R1262 ◽  
Author(s):  
Xiao-Pei Gao ◽  
Israel Rubinstein
Keyword(s):  
Nitric Oxide ◽  
Methyl Ester ◽  
Oral Mucosa ◽  
Biosynthetic Pathway ◽  
Fluorescein Isothiocyanate ◽  
Cheek Pouch ◽  
Site Formation ◽  
Induced Responses ◽  
Hamster Cheek Pouch

The purpose of this study was to determine whether methotrexate modulates bradykinin-induced increase in macromolecular efflux from the in situ oral mucosa and whether this response is mediated by thel-arginine/nitric oxide biosynthetic pathway. Using intravital microscopy, we found that suffusion of methotrexate alone onto the hamster cheek pouch had no significant effects on leaky site formation and increase in clearance of fluorescein isothiocyanate-labeled dextran (molecular mass, 70 kDa). However, methotrexate significantly potentiated bradykinin-induced responses ( P < 0.05). These effects were associated with significant increases in nitrites concentration and guanosine 3′,5′-cyclic monophosphate-like immunoreactivity in the suffusate and were abrogated by N G-nitro-l-arginine methyl ester (l-NAME) but not N G-nitro-d-arginine methyl ester (d-NAME).l-Arginine, but notd-arginine, abolishedl-NAME-induced responses. ZnCI2 and indomethacin had no significant effects on methotrexate-induced responses. Methotrexate had no significant effects on adenosine- and ionomycin-induced increases in macromolecular efflux. Collectively, these data indicate that methotrexate amplifies bradykinin-induced increase in macromolecular efflux from the in situ oral mucosa in a specific, receptor- andl-arginine/nitric oxide biosynthetic pathway-dependent fashion.

Tannic acid elicits neurogenic plasma exudation from the in situ hamster cheek pouch

1998 ◽  
Vol 274 (1) ◽  
pp. R237-R242
Author(s):  
Xiao-Pei Gao
Keyword(s):  
Tannic Acid ◽  
Biosynthetic Pathway ◽  
Fluorescein Isothiocyanate ◽  
Cheek Pouch ◽  
Site Formation ◽  
Hamster Cheek Pouch ◽  
Plasma Exudation ◽  
Synthase Inhibitor

The purpose of this study was to determine whether tannic acid elicits neurogenic plasma exudation from the oral mucosa in vivo and, if so, whether this response is transduced in part by thel-arginine-nitric oxide (NO) biosynthetic pathway. Using intravital microscopy, we found that suffusion of tannic acid elicits significant concentration-dependent leaky site formation and increase in clearance of fluorescein isothiocyanate-dextran (molecular mass 70 kDa) from the in situ hamster cheek pouch ( P < 0.05). These effects are significantly attenuated by two selective, but structurally distinct, nonpeptide neurokinin-1 (NK1) receptor antagonists, CP-96,345 and RP-67580, but not by CP-96,344, the 2R,3R enantiomer of CP-96,345. N G-nitrol-arginine methyl ester (l-NAME), an NO synthase inhibitor, but notd-NAME, significantly attenuates tannic acid-induced responses.l-Arginine, but notd-arginine, reverses the attenuating effects of l-NAME. We conclude that tannic acid elicitsl-arginine-NO biosynthetic pathway-dependent neurogenic plasma exudation from the in situ hamster cheek pouch.

Nitric oxide accounts for histamine-induced increases in macromolecular extravasation

1994 ◽  
Vol 266 (6) ◽  
pp. H2369-H2373 ◽  
Author(s):  
W. G. Mayhan
Keyword(s):  
Nitric Oxide ◽  
Fluorescent Microscopy ◽  
Fluorescein Isothiocyanate ◽  
Cheek Pouch ◽  
Hamster Cheek Pouch ◽  
Before And After ◽  
Subsequent Activation ◽  
Ly 83583

The goal of this study was to determine the role of nitric oxide in histamine-induced increases in macromolecular extravasation in the hamster cheek pouch in vivo. We used intravital fluorescent microscopy and fluorescein isothiocyanate dextran (FITC-dextran; mol wt = 70,000 K) to examine extravasation from postcapillary venules in response to histamine before and after application of an enzymatic inhibitor of nitric oxide, NG-monomethyl-L-arginine (L-NMMA; 1.0 microM). Increases in extravasation of macromolecules were quantitated counting the number of venular leaky sites. Histamine (1.0 and 5.0 microM) increased the number of venular leaky sites from zero (basal conditions) to 11 +/- 1 and 21 +/- 2/0.11 cm2, respectively. Superfusion of L-NMMA (1.0 microM) and LY-83583 (1.0 microM) significantly decreased histamine-induced formation of venular leaky sites, whereas L-arginine (100 microM) potentiated histamine-induced formation of venular leaky sites. In contrast, superfusion of NG-monomethyl-D-arginine (1.0 microM) did not inhibit the formation of venular leaky sites in response to histamine. Thus the findings of the present study suggest that production of nitric oxide, and subsequent activation of guanylate cyclase, plays an important role in macromolecular efflux in vivo in response to histamine.

scholarly journals Grain sorghum dust increases macromolecular efflux from the in situ nasal mucosa

1998 ◽  
Vol 84 (4) ◽  
pp. 1431-1436 ◽  
Author(s):  
Xiao-Pei Gao
Keyword(s):  
Substance P ◽  
Nasal Mucosa ◽  
Fluorescein Isothiocyanate ◽  
Grain Sorghum ◽  
Plasma Exudation ◽  
Substance P Receptor ◽  
Neurokinin 1 ◽  
Dust Extract

The purpose of this study was to determine whether an aqueous extract of grain sorghum dust increases macromolecular efflux from the nasal mucosa in vivo and, if so, whether this response is mediated, in part, by substance P. Suffusion of grain sorghum dust extract on the in situ nasal mucosa of anesthetized hamsters elicits a significant increase in clearance of fluorescein isothiocyanate-labeled dextran (FITC-dextran; mol mass, 70 kDa; P < 0.05). This response is significantly attenuated by CP-96345 and RP-67580, two selective, but structurally distinct, nonpeptide neurokinin 1 (substance P)-receptor antagonists, but not by CP-96344, the 2 R,3 Renantiomer of CP-96345 ( P < 0.05). CP-96345 has no significant effects on adenosine-induced increase in clearance of FITC-dextran from the in situ nasal mucosa. CP-96345 and RP-67580, but not CP-96344, significantly attenuate substance P-induced increases in clearance of FITC-dextran from the in situ nasal mucosa ( P < 0.05). Collectively, these data suggest that grain sorghum dust elicits neurogenic plasma exudation from the in situ nasal mucosa.

Smokeless tobacco-exposed oral keratinocytes increase macromolecular efflux from the in situ oral mucosa

1998 ◽  
Vol 274 (1) ◽  
pp. R104-R111 ◽  
Author(s):  
Israel Rubinstein ◽  
Xiao-Pei Gao ◽  
Sergei Pakhlevaniants ◽  
Dolphine Oda
Keyword(s):  
Oral Mucosa ◽  
Smokeless Tobacco ◽  
Fluorescein Isothiocyanate ◽  
Cheek Pouch ◽  
Oral Keratinocytes ◽  
Hamster Cheek Pouch ◽  
Hoe 140 ◽  
Significant Concentration

The purpose of this study was to determine whether supernatants of cultured human oral keratinocytes (HOK) exposed to an aqueous extract of smokeless tobacco (STE) increase macromolecular efflux from the oral mucosa in vivo and, if so, whether bradykinin mediates in part this response. Subconfluent monolayers of HOK were incubated with STE or media, and supernatants were collected 24, 48, and 72 h thereafter. Using intravital microscopy, we found that suffusion of supernatants of STE- but not media-exposed HOK elicited significant concentration- and time-dependent increases in efflux of fluorescein isothiocyanate-labeled dextran (mol mass 70 kDa) from the in situ hamster cheek pouch ( P < 0.05). These effects were significantly attenuated by HOE-140 and NPC-17647 but not by des-Arg9,[Leu8]-bradykinin. Proteolytic activity was increased in supernatants of STE- but not media-exposed HOK. However, a mixture of leupeptin, Bestatin, anddl-2-mercaptomethyl-3-guanidinoethylthiopropanoic acid had no significant effects on HOK supernatant-induced responses. Collectively, these data suggest that oral keratinocytes modulate smokeless tobacco-induced increase in macromolecular efflux from the in situ oral mucosa in part by elaborating proteases that may account for local bradykinin production.

scholarly journals Dexamethasone attenuates acute macromolecular efflux increase evoked by smokeless tobacco extract

1999 ◽  
Vol 87 (2) ◽  
pp. 619-625 ◽  
Author(s):  
Xiao-Pei Gao ◽  
Syed R. Akhter ◽  
Hiroyuki Ikezaki ◽  
Dennis Hong ◽  
Israel Rubinstein
Keyword(s):  
Oral Mucosa ◽  
Smokeless Tobacco ◽  
Fluorescein Isothiocyanate ◽  
Cheek Pouch ◽  
Site Formation ◽  
Hamster Cheek Pouch ◽  
Acute Increase ◽  
Tobacco Extract

The purpose of this study was to determine whether dexamethasone attenuates the acute increase in macromolecular efflux from the oral mucosa elicited by an aqueous extract of smokeless tobacco (STE) in vivo, and, if so, whether this response is specific. Using intravital microscopy, we found that 20-min suffusion of STE elicited significant, concentration-related leaky site formation and an increase in clearance of fluorescein isothiocyanate-labeled dextran (FITC-dextran; mol mass 70 kDa) from the in situ hamster cheek pouch ( P < 0.05). This response was significantly attenuated by dexamethasone (10 mg/kg iv). Dexamethasone also attenuated the bradykinin-induced leaky site formation and the increase in clearance of FITC-dextran from the cheek pouch. However, it had no significant effects on adenosine-induced responses. Dexamethasone had no significant effects on baseline arteriolar diameter and on bradykinin-induced vasodilation in the cheek pouch. Collectively, these data indicate that dexamethasone attenuates, in a specific fashion, the acute increase in macromolecular efflux from the in situ oral mucosa evoked by short-term suffusion of STE. We suggest that corticosteroids mitigate acute oral mucosa inflammation elicited by smokeless tobacco.

scholarly journals Phasic contractions of rat mesenteric lymphatics increase basal and phasic nitric oxide generation in vivo

2009 ◽  
Vol 297 (4) ◽  
pp. H1319-H1328 ◽  
Author(s):  
H. Glenn Bohlen ◽  
Wei Wang ◽  
Anatoliy Gashev ◽  
Olga Gasheva ◽  
Dave Zawieja
Keyword(s):  
Nitric Oxide ◽  
Relaxation Mechanism ◽  
Lymph Flow ◽  
Lymphatic Endothelium ◽  
Contraction Frequency ◽  
Diastolic Relaxation ◽  
Intravenous Saline ◽  
First Time

Multiple investigators have shown interdependence of lymphatic contractions on nitric oxide (NO) activity by pharmacological and traumatic suppression of endothelial NO synthase (eNOS). We demonstrated that lymphatic diastolic relaxation is particularly sensitive to NO from the lymphatic endothelium. The predicted mechanism is shear forces produced by the lymph flow during phasic pumping, activating eNOS in the lymphatic endothelium to produce NO. We measured [NO] during phasic contractions using microelectrodes on in situ mesenteric lymphatics in anesthetized rats under basal conditions and with an intravenous saline bolus (0.5 ml/100 g) or infusion (0.5 ml·100 g−1·h−1). Under basal conditions, [NO] measured on the tubular portions of the lymphatics was ∼200–250 nM, slightly higher than in the adjacent adipocyte microvasculature, whereas [NO] measured on the lymphatic bulb surface was ∼400 nM. Immunohistochemistry of eNOS in isolated lympathics indicated a much greater expression in the lymph valves and surrounding bulb area than in the tubular regions. During phasic lymphatic contractions, the valve and tubular [NO] increased with each contraction, and during intravenous saline infusion, [NO] increased in proportion to the contraction frequency and, presumably, lymph flow. The partial blockade of eNOS over ∼1 cm length with Nω-nitro-l-arginine methyl ester lowered the [NO]. These in vivo data document for the first time that both valvular and tubular lymphatic segments increase NO generation during each phasic contraction and that [NO] summated with increased contraction frequency. The combined data predict regional variations in eNOS and [NO] in the tubular and valve areas, plus the summated NO responses dependent on contraction frequency provide for a complex relaxation mechanism involving NO.

Role of Endothelial Nitric Oxide Synthase as a Trigger and Mediator of Isoflurane-induced Delayed Preconditioning in Rabbit Myocardium

2005 ◽  
Vol 103 (1) ◽  
pp. 74-83 ◽  
Author(s):  
Pascal C. Chiari ◽  
Martin W. Bienengraeber ◽  
Dorothee Weihrauch ◽  
John G. Krolikowski ◽  
Judy R. Kersten ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Methyl Ester ◽  
Nitric Oxide Synthase ◽  
Infarct Size ◽  
Coronary Occlusion ◽  
Nos Inhibitor ◽  
Neuronal Nos ◽  
Oxide Synthase ◽  
Inducible Nos

Background Isoflurane produces delayed preconditioning in vivo. The authors tested the hypothesis that endothelial, inducible, or neuronal nitric oxide synthase (NOS) is a trigger or mediator of this protective effect. Methods In the absence or presence of exposure to isoflurane (1.0 minimum alveolar concentration) 24 h before experimentation, pentobarbital-anesthetized rabbits (n = 128) instrumented for hemodynamic measurement received 0.9% saline (control), the nonselective NOS inhibitor N-nitro-l-arginine methyl ester (10 mg/kg), one of two of the selective inducible NOS antagonists aminoguanidine (300 mg/kg) or 1400W (0.5 mg/kg), or the selective neuronal NOS inhibitor 7-nitroindazole (50 mg/kg) administered before exposure to isoflurane (trigger; day 1) or left anterior descending coronary artery occlusion (mediator; day 2). All rabbits underwent 30 min of coronary occlusion followed by 3 h of reperfusion. Tissue samples for reverse-transcription polymerase chain reaction and immunohistochemistry were also obtained in the presence or absence of N-nitro-l-arginine methyl ester with or without isoflurane pretreatment. Results Isoflurane significantly (P &lt; 0.05) reduced infarct size (23 +/- 5% [mean +/- SD] of the left ventricular area at risk; triphenyltetrazolium chloride staining) as compared with control (42 +/- 7%). N-nitro-l-arginine methyl ester administered before isoflurane or coronary occlusion abolished protection (49 +/- 7 and 43 +/- 10%, respectively). Aminoguanidine, 1400W, and 7-nitroindazole did not alter infarct size or affect isoflurane-induced delayed preconditioning. Isoflurane increased endothelial but not inducible NOS messenger RNA transcription and protein translation immediately and 24 h after administration of the volatile agent. Pretreatment with N-nitro-l-arginine methyl ester attenuated isoflurane-induced increases in endothelial NOS expression. Conclusions The results suggest that endothelial NOS but not inducible or neuronal NOS is a trigger and mediator of delayed preconditioning by isoflurane in vivo.

scholarly journals Shear-induced modulation of vasoconstriction in the hepatic artery and portal vein by nitric oxide

1998 ◽  
Vol 274 (2) ◽  
pp. G253-G260 ◽  
Author(s):  
M. Paula Macedo ◽  
W. Wayne Lautt
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Shear Stress ◽  
Methyl Ester ◽  
Portal Vein ◽  
Hepatic Artery ◽  
Nerve Stimulation ◽  
Perfusion Pressure ◽  
No Synthase

The effect of shear stress on nitric oxide (NO)-mediated suppression of sympathetic nerve (2–6 Hz)- and norepinephrine (0.5 μg ⋅ kg−1 ⋅ min−1)-induced vasoconstriction in the hepatic artery (HA) and portal vein (PV) was studied using a perfusion circuit to regulate blood pressure and flow in the cat liver in situ. Holding flow constant resulted in increased shear stress during constriction; holding pressure steady prevented changes in shear stress. When shear stress was allowed to rise, the vasoconstriction (indicated by elevation in perfusion pressure) in response to nerve stimulation and norepinephrine was significantly potentiated after NO synthase blockade using N G-nitro-l-arginine methyl ester (l-NAME, 2.5 mg/kg iv) in both the HA and PV (response to nerves: HA control 28.8 ± 6.5 mmHg,l-NAME 62.7 ± 14.6 mmHg; PV control 1.5 ± 0.5 mmHg,l-NAME 3.3 ± 0.5 mmHg; response to norepinephrine: HA control 32.4 ± 9.0 mmHg, l-NAME 60.3 ± 8.0 mmHg; PV control 1.3 ± 0.3 mmHg,l-NAME 3.4 ± 0.7 mmHg). The potentiation was reversed byl-arginine (75 mg/kg). When shear stress was held constant by maintaining constant perfusion pressure, l-NAME did not cause potentiation of vasoconstriction. The data are consistent with the hypothesis that elevated shear stress in the hepatic blood vessels leads to NO-dependent postjunctional modulation of vasoconstriction.

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