Innervation and neurokinin receptors during angiogenesis in the rat sponge granuloma

1996 ◽  
Vol 28 (11) ◽  
pp. 759-769 ◽  
Author(s):  
D. A. Walsh ◽  
D. -E. Hu ◽  
P. I. Mapp ◽  
J. M. Polak ◽  
D. R. Blake ◽  
...  
Keyword(s):  
1998 ◽  
Vol 160 (2) ◽  
pp. 298-298 ◽  
Author(s):  
Michael R. Ruggieri

1988 ◽  
Vol 22 (1-2) ◽  
pp. 191 ◽  
Author(s):  
K. Yashpal ◽  
T.V. Dam ◽  
R. Quirion

Author(s):  
Brian P. Enright ◽  
Michael W. Leach ◽  
Georges Pelletier ◽  
Fernand LaBrie ◽  
Barry S. McIntyre ◽  
...  

Neuropeptides ◽  
1987 ◽  
Vol 10 (1) ◽  
pp. 43-54 ◽  
Author(s):  
G. Drapeau ◽  
P. D'Orléans-Juste ◽  
S. Dion ◽  
N.-E. Rhaleb ◽  
N.-E. Rouissi ◽  
...  

Author(s):  
DOMENICO REGOLI ◽  
NOURREDINE ROUISSI ◽  
PEDRO D'ORLÉANS-JUSTE
Keyword(s):  

1995 ◽  
Vol 268 (1) ◽  
pp. G161-G170 ◽  
Author(s):  
E. E. Daniel ◽  
M. B. Parrish ◽  
E. G. Watson ◽  
J. E. Fox-Threlkeld ◽  
D. Regoli ◽  
...  

This study sought to determine which tachykinin receptors were involved in contractile responses of circular muscle to tachykinins infused into isolated segments of canine ileum. Selective agonists for neurokinin receptors NK1 and NK2 as well as for substance P (SP) and neurokinin A (NKA) were infused, and selective antagonists against NK1, NK2, and NK3 receptors were tested. The responses to a submaximal concentration of NKA were reduced by a selective NK2 antagonist, SR-48968, and abolished by a combination of this antagonist with an NK1 antagonist, either CP-96,345 or RP-67580. The selective NK2 agonist, [Nle10]NKA-(4-10), had low potency. We concluded that NKA acted on typical NK2 receptors and that is action was potentiated by its additional action on NK1 receptors. Neither the contractile responses to SP nor those to [Sar9,Met(O2)11]SP given in submaximal concentrations were inhibited by CP-96,345 or RP-67580, either alone or together with SR-48968. Indeed, the two NK1-selective antagonists potentiated responses to the selective NK1 agonist, [Sar9,Met(O2)11]SP, an effect attributed to previously demonstrated prejunctional inhibitory action of the agonist. The selective NK3 agonist, succinyl-[Asp6,N-Me-Phe8]SP-(6-11), was not effective as a contractile agent, even after block of nitric oxide synthase with N omega-nitro-L-arginine. The selective NK3 antagonist, R-487, was also ineffective in blocking responses to SP. Studies with an antagonist to H1 histamine receptors suggested that contractile actions of SP did not involve histamine release from mast cells. We concluded that, in addition to typical NK1 and NK2 receptors activated by NKA and a prejunctional inhibitory receptor activated by SP and [Sar9,Met(O2)11]SP, another tachykinin receptor existed on canine ileum to initiate contractions. It is not a typical NK1, NK2, or NK3 receptor.


2003 ◽  
Vol 285 (4) ◽  
pp. C945-C958 ◽  
Author(s):  
Fabien Schmidlin ◽  
Dirk Roosterman ◽  
Nigel W. Bunnett

Tachykinins interact with three neurokinin receptors (NKRs) that are often coexpressed by the same cell. Cellular responses to tachykinins depend on the NKR subtype that is activated. We compared the colocalization of NK1R and NK3R with β-arrestins 1 and 2, which play major roles in receptor desensitization, endocytosis, and signaling. In cells expressing NK1R, the selective agonist Sar-Met-substance P induced rapid translocation of β-arrestins 1 and 2 from the cytosol to the plasma membrane and then endosomes, indicative of interaction with both isoforms. In contrast, the NK3R interacted transiently with only β-arrestin 2 at the plasma membrane. Despite these differences, both NK1R and NK3R similarly desensitized, internalized, and activated MAP kinases. Because interactions with β-arrestins can explain differences in the rate of receptor resensitization, we compared resensitization of agonist-induced Ca2+ mobilization. The NK1R resensitized greater than twofold more slowly than the NK3R. Replacement of intracellular loop 3 and the COOH tail of the NK1R with comparable domains of the NK3R diminished colocalization of the NK1R with β-arrestin 1 and accelerated resensitization to that of the NK3R. Thus loop 3 and the COOH tail specify colocalization of the NK1R with β-arrestin 1 and determine the rate of resensitization.


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