Gastrin-releasing peptide directly releases pepsinogen from guinea pig chief cells

1990 ◽  
Vol 259 (5) ◽  
pp. G760-G766 ◽  
Author(s):  
S. Fiorucci ◽  
K. E. McArthur
Keyword(s):  
Substance P ◽  
Guinea Pig ◽  
Receptor Antagonist ◽  
Fold Increase ◽  
Chief Cells ◽  
Gastrin Releasing Peptide ◽  
Basal Release ◽  
Substance P Receptor ◽  
Bombesin Receptor ◽  
Muscarinic Agents

Gastrin-releasing peptide (GRP) and bombesin can stimulate pepsinogen release by both gastrin-dependent and -independent mechanisms. Using isolated guinea pig gastric chief cells, we determined that GRP can act directly on the guinea pig chief cell to cause pepsinogen release. GRP and bombesin stimulated a 2.5- to 3-fold increase in pepsinogen release above basal release. Substance P also stimulated a small but significant increase in pepsinogen release. No gastrin immunoreactivity was detected in the supernatants of cells stimulated with up to 1 microM GRP or bombesin or 1 mM carbachol. GRP-stimulated pepsinogen release was completely inhibited by GRP/bombesin receptor agonists as well as substance P receptor antagonist but not by antagonists to receptors for gastrin, the octapeptide of cholecystokinin (CCK-8), secretin, vasoactive intestinal peptide (VIP), or muscarinic agents. Substance P-stimulated pepsinogen release was completely inhibited by substance P receptor antagonist but not by GRP/bombesin receptor antagonists. An additive effect on pepsinogen release was seen when GRP was combined with maximally effective concentrations of adenosine 3',5'-cyclic monophosphate (cAMP)-mediated agents (VIP, secretin, 8-BrcAMP) but not with calcium-mediated agents (carbachol, CCK-8, gastrin). These results indicate that GRP can directly stimulate pepsinogen release from guinea pig chief cells by a specific GRP receptor that mobilizes intracellular calcium.

Dual effects of PACAP on guinea pig gallbladder muscle via PACAP-preferring and VIP/PACAP-preferring receptors

1997 ◽  
Vol 272 (6) ◽  
pp. G1433-G1438 ◽  
Author(s):  
H. P. Parkman ◽  
A. P. Pagano ◽  
J. P. Ryan
Keyword(s):  
Substance P ◽  
Adenylate Cyclase ◽  
Guinea Pig ◽  
Receptor Antagonist ◽  
Direct Action ◽  
Inhibitory Effects ◽  
Relaxant Effect ◽  
Pituitary Adenylate Cyclase ◽  
Substance P Receptor ◽  
Dose Dependent

The aims of this study were to determine the effect and mechanism of action of pituitary adenylate cyclase-activating peptide (PACAP) on gallbladder muscle. Guinea pig gallbladder muscle strips were studied isometrically. In noncontracted muscle strips, PACAP-27 and PACAP-38 caused dose-dependent contractions, whereas vasoactive intestinal peptide (VIP) caused dose-dependent relaxation. PACAP-27 contractions were resistant to tetrodotoxin, atropine, and the substance P receptor antagonist [D-Arg1,D-Trp7,9,Leu11]substance P (Spantide) but were inhibited by the selective PACAP receptor antagonist PACAP-(6-38) and slightly increased with the VIP receptor antagonist [4-chloro-D-Phe6,Leu17]VIP. In cholecystokinin-precontracted muscle strips, both VIP and PACAP caused relaxations. This relaxant effect of PACAP-27 was inhibited by PACAP-(6-38) and [4-chloro-D-Phe6,Leu17]VIP, but not by tetrodotoxin. These studies suggest that PACAP has dual excitatory and inhibitory effects on guinea pig gallbladder muscle. The contractile effect of PACAP is a direct action on muscle through PACAP-preferring receptors. The relaxant effect of PACAP is seen in precontracted muscle strips and mediated through VIP/ PACAP-preferring receptors.

UVR-B-induced NKR-1 Expression in Ocular Tissues is blocked by Substance P Receptor Antagonist Fosaprepitant in the Exposed as well as Unexposed Partner Eye

2020 ◽  
pp. 1-13
Author(s):  
Janine Gross ◽  
Alfred R. Wegener ◽  
Martin Kronschläger ◽  
Carl-Ludwig Schönfeld ◽  
Frank G. Holz ◽  
...  
Keyword(s):  
Substance P ◽  
Receptor Antagonist ◽  
Ocular Tissues ◽  
Substance P Receptor

Somatostatin inhibits VIP-stimulated amylase release from perifused guinea pig pancreatic acini

1988 ◽  
Vol 254 (2) ◽  
pp. G217-G223 ◽  
Author(s):  
P. Singh ◽  
I. Asada ◽  
A. Owlia ◽  
T. J. Collins ◽  
J. C. Thompson
Keyword(s):  
Guinea Pig ◽  
Fold Increase ◽  
Optimal Conditions ◽  
Amylase Release ◽  
Pancreatic Acini ◽  
In Vitro System ◽  
Basal Release ◽  
Perifusion System ◽  
Chamber Size

We have examined the direct effect of somatostatin (SRIF) on basal and stimulated amylase release from guinea pig pancreatic acini using the in vitro method of continuous perifusion. The optimal conditions of flow rate, chamber size, acinar cell volume per chamber, and period of secretagogue infusion were defined for the perifusion system. The kinetic profile of amylase release in response to cholecystokinin-octapeptide (CCK-8), vasoactive intestinal peptide (VIP), and SRIF was studied. Under optimal conditions, the acini were found to remain equally responsive to an ED50 dose of CCK-8 (0.5-0.8 nM) for 12 h of perifusion. The duration of amylase response to any given dose of CCK-8, given for the optimal period of 5 min, was 80-100 min. The total amylase released minus the basal release divided by 90 min (delta response) in response to the maximum effective (Maxeff) dose of CCK-8 (100 nM) was 14,667 +/- 1,433 U/l (amounting to a 10-fold increase compared with basal values). When compared with the amount of total delta amylase released in response to the Maxeff dose of CCK, the total amylase released in response to the Maxeff doses of SRIF (1 microM) and VIP (10 nM) was 10-21% and 51-59%, respectively. SRIF (100 nM) significantly decreased VIP- (0.1-1.0 nM) stimulated amylase release by 45-70% in the perifusion method of study but had no significant effect on the CCK-stimulated amylase release. This suggests that the perifusion method can be used for investigating the mechanism of SRIF-mediated inhibition of VIP effects on amylase release in an in vitro system.

scholarly journals Roles for substance P and gastrin-releasing peptide as neurotransmitters released by primary afferent pruriceptors

2013 ◽  
Vol 109 (3) ◽  
pp. 742-748 ◽  
Author(s):  
Tasuku Akiyama ◽  
Mitsutoshi Tominaga ◽  
Auva Davoodi ◽  
Masaki Nagamine ◽  
Kevin Blansit ◽  
...  
Keyword(s):  
Substance P ◽  
Receptor Antagonist ◽  
Sensory Neurons ◽  
Intrathecal Administration ◽  
Primary Sensory Neurons ◽  
Gastrin Releasing Peptide ◽  
Behavioral Studies ◽  
Neurokinin 1 ◽  
Protease Activated Receptor 2 ◽  
Grp Receptor

Recent studies support roles for neurokinin-1 (NK-1) and gastrin-releasing peptide (GRP) receptor-expressing spinal neurons in itch. We presently investigated expression of substance P (SP) and GRP in pruritogen-responsive primary sensory neurons and roles for these neuropeptides in itch signaling. Responses of dorsal root ganglion (DRG) cells to various pruritogens were observed by calcium imaging. DRG cells were then processed for SP, GRP, and isolectin B-4 (IB4; a marker for nonpeptidergic neurons) immunofluorescence. Of pruritogen-responsive DRG cells, 11.8–26.8%, 21.8–40.0%, and 21.4–26.8% were immunopositive for SP, GRP, and IB4, respectively. In behavioral studies, both systemic and intrathecal administration of a NK-1 receptor antagonist significantly attenuated scratching evoked by chloroquine and a protease-activated receptor 2 agonist, SLIGRL, but not histamine, bovine adrenal medulla peptide 8-22 (BAM8-22), or serotonin. Systemic or intrathecal administration of a GRP receptor antagonist attenuated scratching evoked by chloroquine and SLIGRL but not BAM8-22 or histamine. The GRP receptor antagonist enhanced scratching evoked by serotonin. These results indicate that SP and GRP expressed in primary sensory neurons are partially involved as neurotransmitters in histamine-independent itch signaling from the skin to the spinal cord.

Tachykinins mediate slow excitatory postsynaptic transmission in guinea pig sphincter of Oddi ganglia

2001 ◽  
Vol 281 (2) ◽  
pp. G357-G364 ◽  
Author(s):  
Brian P. Manning ◽  
Gary M. Mawe
Keyword(s):  
Substance P ◽  
Guinea Pig ◽  
Receptor Antagonist ◽  
Synaptic Input ◽  
Intracellular Recording ◽  
Small Diameter ◽  
Sphincter Of Oddi ◽  
Receptor Desensitization ◽  
Afferent Fibers ◽  
Excitatory Synaptic Input

Intracellular recording techniques were used to test whether tachykinins could be mediators of slow excitatory postsynaptic potentials (EPSPs) in guinea pig sphincter of Oddi (SO) ganglia. Application of the tachykinin substance P (SP) onto SO neurons caused a prolonged membrane depolarization that was reminiscent of the slow EPSP in these cells. Pressure ejection of the neurokinin 3 (NK3) receptor-specific agonist senktide caused a similar depolarization; however, no responses were detected on application of NK1 or NK2 receptor agonists. The NK3 receptor antagonist SR-142801 (100 nM) significantly inhibited both SP-induced depolarization and the stimulation-evoked slow EPSP, as did NK3 receptor desensitization with senktide. Capsaicin, which causes the release of SP from small-diameter afferent fibers, induced a depolarization that was similar to the evoked slow EPSP in both amplitude and duration. The capsaicin-induced depolarization was significantly attenuated in the presence of SR-142801. These data indicate that tachykinins, released from extrinsic afferent fibers, act via NK3 receptors to provide slow excitatory synaptic input to SO neurons.

BRAIN PENETRATION OF APREPITANT, A SUBSTANCE P RECEPTOR ANTAGONIST, IN FERRETS

2003 ◽  
Vol 31 (6) ◽  
pp. 785-791 ◽  
Author(s):  
Su-Er W. Huskey ◽  
Brian J. Dean ◽  
Ray Bakhtiar ◽  
Rosa I. Sanchez ◽  
F. David Tattersall ◽  
...  
Keyword(s):  
Substance P ◽  
Receptor Antagonist ◽  
Brain Penetration ◽  
Substance P Receptor
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