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Vol. 84, Issue 1, 169-176, January 1998
Department of Medicine, University of Illinois at Chicago, and West Side Department of Veterans Affairs Medical Center, Chicago, Illinois 60612
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 the
L-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
NG-L-arginine
methyl ester (L-NAME), but not
NG-D-arginine
methyl ester, significantly attenuated ovalbumin-induced responses.
L-Arginine, but not
D-arginine, abolished the effects of
L-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 the
L-arginine/nitric oxide
biosynthetic pathway.
microcirculation; inflammation; bradykinin; nitric oxide; allergic rhinitis
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