IV. Neural regulation of gastrointestinal smooth muscle

1998 ◽  
Vol 275 (1) ◽  
pp. G1-G7 ◽  
Author(s):  
Kenton M. Sanders

G protein-coupled receptors receive many of the neural, hormonal, and paracrine inputs to gastrointestinal (GI) smooth muscle cells. This article examines the major G protein-coupled receptors, G proteins, and effectors that mediate responses to enteric neuromuscular transmitters. Excitatory transmitters primarily couple through Gq/11 and Gi/Goproteins and elicit responses via formation of inositol trisphosphate and diacylglycerol and inhibition of adenylyl cyclase. Several inhibitory transmitters couple through Gs and activation of adenylyl cyclase. There are interesting examples, however, of inhibitory transmitters apparently using pathways regulated by Gq/11 to elicit responses by localized Ca2+ release and activation of Ca2+-dependent ion channels. G protein-coupled receptors may also be differentially expressed by smooth muscle cells and interstitial cells of Cajal, which may increase the diversity of responses and allow specialized innervation of GI muscle tissues.

2002 ◽  
Vol 283 (2) ◽  
pp. C446-C455 ◽  
Author(s):  
Laure Voisin ◽  
Sylvain Foisy ◽  
Edith Giasson ◽  
Chantal Lambert ◽  
Pierre Moreau ◽  
...  

The epidermal growth factor receptor (EGFR) was recently identified as a signal transducer of G protein-coupled receptors (GPCRs). In this study, we have examined the contribution of EGFR transactivation to the growth-promoting effect of GPCRs on vascular smooth muscle cells. Activation of the Gq-coupled ANG II receptor or Gi-coupled lysophosphatidic acid receptor resulted in increased tyrosine phosphorylation and activation of EGFR. Specific inhibition of EGFR kinase activity by tyrphostin AG-1478 or expression of a dominant-negative EGFR mutant abolished this response. Importantly, inhibition of EGFR function strongly attenuated the global stimulation of protein synthesis by GPCR agonists in vitro in cultured aortic smooth muscle cells and in vivo in the rat aorta and in small resistance arteries. The growth inhibition was associated with a marked reduction of extracellular signal-regulated kinase and phosphoinositide 3-kinase pathway activity and the resulting suppression of eukaryotic translation initiation factor 4E and 4E binding protein 1 phosphorylation. Our results demonstrate that EGFR transactivation is a physiologically relevant action of GPCRs linked to translational control and protein synthesis.


2002 ◽  
Vol 34 (10) ◽  
pp. 1399-1409 ◽  
Author(s):  
Karsten Peppel ◽  
Lisheng Zhang ◽  
Tam T.T. Huynh ◽  
Xuewei Huang ◽  
Anne Jacobson ◽  
...  

1984 ◽  
Vol 246 (3) ◽  
pp. G305-G315 ◽  
Author(s):  
E. E. Daniel ◽  
V. Posey-Daniel

The structures of the lower esophageal sphincter (LES) and body circular muscle (BCM) from opossum were compared as to neural and muscular structures and the structural relations of interstitial cells of Cajal to nerves and muscle cells. Both LES and BCM were densely innervated by nerves with varicosities containing many small agranular vesicles and a few large granular vesicles. These nerves were more closely related structurally to the interstitial cells of Cajal than to smooth muscle cells. More gap junctions were observed between smooth muscle cells and between interstitial cells of Cajal and smooth muscle cells in BCM than in LES. Those between smooth muscle cells were larger in BCM. Complete relaxation of the LES strip by isoproterenol reduced these differences but did not eliminate them. The finding that interstitial cells of Cajal often had gap-junction contacts to smooth muscle and close associations with nerves is consistent with the hypothesis that interstitial cells are intercalated between the nerves and muscles and may mediate nerve responses. These findings also suggest that LES muscle cells may be less well coupled electrically than BCM muscle cells.


2006 ◽  
Vol 99 (2) ◽  
pp. 132-139 ◽  
Author(s):  
Stéphanie Gayral ◽  
Paul Déléris ◽  
Karine Laulagnier ◽  
Muriel Laffargue ◽  
Jean-Pierre Salles ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document