scholarly journals Epithelium-dependent regulation of airways smooth muscle function. A histamine-nitric oxide pathway

1998 ◽  
Vol 7 (6) ◽  
pp. 409-411 ◽  
Author(s):  
Konstantinos Gourgoulianis ◽  
Zoe Iliodromitis ◽  
Apostolia Hatziefthimiou ◽  
Paschalis-Adam Molyvdas

The airway epithelium is responsible for the production of a number of arachidonic acid and nonprostanoid inhibitory factors. Epithelium synthesises nitric oxide (NO) which may be important in regulating the function of airways smooth muscles. We studiedin vitrothe effect of histamine (100 nM100 μ M) which increases the NO release on rabbit airway smooth muscles induced by 80 mM KCl in the presence or not of 10-5Methylene blue (MB) (inactivator of guanylate cyclase) or N(G)-monomethyl L-arginine (L-NMMA), a NOS inhibitor. All experiments were done in tracheal muscle strips from 28 rabbits with epithelium and after epithelium removal. The additional use of histamine (1 μ M) on KCl contraction induced a relaxation of 10% of the initial contraction. The additional use of L-NMMA decreased the relaxation to 5% of initial contraction. MB rather than L-NMMA increased the contraction significantly(p<0.01). Epithelium removal increased the contraction induced by KCl (80 mM) and histamine (1 μ M) by about 30%(p<0.001). NO release especially from epithelium regulates the airways smooth muscle functions. Damage to the epithelium may contribute to an increase in airways sensitivity, observed in asthma.

1988 ◽  
Vol 254 (1) ◽  
pp. G124-G129 ◽  
Author(s):  
D. L. Vermillion ◽  
S. M. Collins

We examined in vitro changes in contractility of jejunal longitudinal muscle strips in rats infected with the nematode parasite Trichinella spiralis. Length-passive tension relationships were unchanged. However, muscle from infected rats on days 5 and 6 postinfection (PI) generated maximal active tension induced by carbachol at significantly less stretch (39.9 +/- 1.0 and 34.3 +/- 6.3%, respectively) than control tissues (66.0 +/- 2.3%). In infected rats on day 5 PI, the maximum tension generated by carbachol (1.6 +/- 0.4 g/mm2) and by 5-hydroxytryptamine (5-HTP) (2.6 +/- 0.1 g/mm2) was significantly greater than in control tissue (0.5 +/- 0.2 g/mm2). On removal of calcium from the medium, responses of muscle from control and infected rats were reduced in a proportionate manner. The increased responsiveness to carbachol and 5-HTP was maximal by day 5 PI and was associated with a decrease in the ED50 value for 5-HTP but not for carbachol. All changes were reversed by 23 days PI. These results indicate that T. spiralis infection in the rat is associated with alterations in jejunal longitudinal smooth muscle function.


2001 ◽  
Vol 281 (2) ◽  
pp. L469-L474 ◽  
Author(s):  
Christopher N. Fortner ◽  
Richard M. Breyer ◽  
Richard J. Paul

Substance P (SP) and ATP evoke transient, epithelium-dependent relaxation of constricted mouse tracheal smooth muscle. Relaxation to either SP or ATP is blocked by indomethacin, but the specific eicosanoid(s) involved have not been definitively identified. SP and ATP are reported to release PGE2 from airway epithelium in other species, suggesting PGE2 as a likely mediator in epithelium-dependent airway relaxation. Using mice homozygous for a gene-targeted deletion of the EP2 receptor [EP2(−/−)], one of the PGE2 receptors, we tested the hypothesis that PGE2 is the primary mediator of relaxation to SP or ATP. Relaxation in response to SP or ATP was significantly reduced in tracheas from EP2(−/−) mice. There were no differences between EP2(−/−) and wild-type tracheas in their physical dimensions, contraction to ACh, or relaxation to isoproterenol, thus ruling out any general alterations of smooth muscle function. There were also no differences between EP2(−/−) and wild-type tracheas in basal or stimulated PGE2 production. Exogenous PGE2 produced significantly less relaxation in EP2(−/−) tracheas compared with the wild type. Taken together, this experimental evidence supports the following two conclusions: EP2 receptors are of primary importance in airway relaxation to PGE2 and relaxation to SP or ATP is mediated through PGE2 acting on EP2 receptors.


2008 ◽  
Vol 7 (3) ◽  
pp. 216
Author(s):  
H. Ertemi ◽  
D. Lau ◽  
F.H. Mumtaz ◽  
D.P. Mikhailidis ◽  
C.S. Thompson

1994 ◽  
Vol 21 (3) ◽  
pp. 430-440 ◽  
Author(s):  
Piero Portincasa ◽  
Agostino Di Ciaula ◽  
Giuseppe Baldassarre ◽  
Vincenzo Palmieri ◽  
Antonia Gentile ◽  
...  

2001 ◽  
Vol 165 (4) ◽  
pp. 1310-1315 ◽  
Author(s):  
ROBERT R. BYRNE ◽  
GERARD D. HENRY ◽  
DINESH S. RAO ◽  
T.T.T. HUYNH ◽  
ANNE M. PIPPEN ◽  
...  

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