Comparative Study of pA2 Values of Pirenzepine and Atropine for Guinea-Pig Gastric Fundus and Gastric Smooth Muscle

Pharmacology ◽  
1984 ◽  
Vol 29 (6) ◽  
pp. 329-335 ◽  
Author(s):  
Del Tacca ◽  
G. Soldani ◽  
C. Bernardini ◽  
E. Martinotti
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Comparative Study ◽  
Gastric Fundus ◽  
Gastric Smooth Muscle

Functional differences of Na+/Ca2+ exchanger expression in Ca2+ transport system of smooth muscle of guinea pig stomach

2005 ◽  
Vol 83 (8-9) ◽  
pp. 791-797 ◽  
Author(s):  
Yasushi Sakai ◽  
Hiroki Kinoshita ◽  
Keiichirou Saitou ◽  
Ikuo Homma ◽  
Koji Nobe ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Plasma Membrane ◽  
Guinea Pig ◽  
Gastric Fundus ◽  
Relaxation Cycle ◽  
Gastric Smooth Muscle ◽  
Guinea Pig Stomach ◽  
And Function ◽  
The Relationship ◽  
Ionophore Monensin

The plasma membrane ATP-dependent Ca2+ pump and the Na+/Ca2+ exchanger (NCX) are the major means of Ca2+ extrusion in smooth muscle. However, little is known regarding distribution and function of the NCX in guinea pig gastric smooth muscle. The expression pattern and distribution of NCX isoforms suggest a role as a regulator of Ca2+ transport in cells. Na+ pump inhibition and the consequent to removal of K+ caused gradual contraction in fundus. In contrast, the response was significantly less in antrum. Western blotting analysis revealed that NCX1 and NCX2 are the predominant NCX isoforms expressed in stomach, the former was expressed strongly in antrum, whereas the latter displayed greater expression in fundus. Isolated plasma membrane fractions derived from gastric fundus smooth muscle were also investigated to clarify the relationship between NCX protein expression and function. Na+-dependent Ca2+ uptake increased directly with Ca2+ concentration. Ca2+ uptake in Na+-loaded vesicles was markedly elevated in comparison with K+-loaded vesicles. Additionally, Ca2+ uptake by the Na+- or K+-loaded vesicles was substantially higher in the presence of A23187 than in its absence. The result can be explained based on the assumption that Na+ gradients facilitate downhill movement of Ca2+. Na+-dependent Ca2+ uptake was abolished by the monovalent cationic ionophore, monensin. NaCl enhanced Ca2+ efflux from vesicles, and this efflux was significantly inhibited by gramicidin. Results documented evidence that NCX2 isoform functionally contributes to Ca2+ extrusion and maintenance of contraction-relaxation cycle in gastric fundus smooth muscle.Key words: stomach, smooth muscle, Na+/Ca2+ exchanger (NCX), NCX2.

Identification of neurotransmitters by selective protection of postjunctional receptors

1990 ◽  
Vol 258 (1) ◽  
pp. G103-G106
Author(s):  
J. R. Grider
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Gastric Fundus ◽  
Membrane Receptors ◽  
Field Stimulation ◽  
Dibutyryl Camp ◽  
Selective Protection ◽  
Gastric Smooth Muscle ◽  
Selective Ligands ◽  
Before And After

The neurotransmitter responsible for relaxation of gastric smooth muscle was identified by a technique involving the use of selective ligands to protect postjunctional receptors combined with inactivation of all other receptors with N-ethylmaleimide (NEM). Relaxation in response to field stimulation (80 V, 1 ms, 0.5-8 Hz) and to maximally effective concentrations of vasoactive intestinal peptide (VIP; 1 microM), ATP (1 mM), isoproterenol (1 mM), dibutyryl adenosine 3',5'-cyclic monophosphate (cAMP; 1 mM), and forskolin (1 microM) was measured in muscle strips from guinea pig gastric fundus before and after treatment with NEM (5 microM) for 1 h. Protection of VIP receptors with VIP or the VIP antagonist VIP10-28 fully protected relaxation induced by VIP and by field stimulation, but did not protect relaxation induced by ATP or isoproterenol. Protection of ATP receptors with ATP protected only the response to ATP, but did not protect the response to field stimulation, VIP, or isoproterenol. Relaxation induced by either forskolin or dibutyryl cAMP was not altered by treatment with NEM alone or in the presence of protective ligands, indicating that at the concentrations used NEM inactivated membrane receptors without affecting intracellular relaxation mechanisms. These studies indicate that VIP but not ATP is the neurotransmitter responsible for neurally induced relaxation in the gastric fundus.

scholarly journals Adiponectin Exerts Peripheral Inhibitory Effects on the Mouse Gastric Smooth Muscle through the AMPK Pathway

2020 ◽  
Vol 21 (24) ◽  
pp. 9617
Author(s):  
Eglantina Idrizaj ◽  
Rachele Garella ◽  
Silvia Nistri ◽  
Alfonso Dell’Accio ◽  
Emanuele Cassioli ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Multidisciplinary Approach ◽  
Gastric Fundus ◽  
Inhibitory Effects ◽  
Immunofluorescence Analysis ◽  
Synthesis Inhibitor ◽  
Ampk Signaling ◽  
Gastric Smooth Muscle ◽  
Treatment Of Obesity ◽  
Amp Activated Protein Kinase

Some adipokines, such as adiponectin (ADPN), other than being implicated in the central regulation of feeding behavior, may influence gastric motor responses, which are a source of peripheral signals that also influence food intake. The present study aims to elucidate the signaling pathways through which ADPN exerts its actions in the mouse gastric fundus. To this purpose, we used a multidisciplinary approach. The mechanical results showed that ADPN caused a decay of the strip basal tension, which was abolished by the nitric oxide (NO) synthesis inhibitor, L-NG-nitro arginine (L-NNA). The electrophysiological experiments confirmed that all ADPN effects were abolished by L-NNA, except for the reduction of Ca2+ current, which was instead prevented by the inhibitor of AMP-activated protein kinase (AMPK), dorsomorphin. The activation of the AMPK signaling by ADPN was confirmed by immunofluorescence analysis, which also revealed the ADPN R1 receptor (AdipoR1) expression in glial cells of the myenteric plexus. In conclusion, our results indicate that ADPN exerts an inhibitory action on the gastric smooth muscle by acting on AdipoR1 and involving the AMPK signaling pathway at the peripheral level. These findings provide novel bases for considering AMPK as a possible pharmacologic target for the potential treatment of obesity and eating disorders.

Smooth muscle cells from guinea pig stomach possess high-affinity galanin receptors that mediate relaxation

1994 ◽  
Vol 266 (5) ◽  
pp. G839-G845 ◽  
Author(s):  
Z. F. Gu ◽  
T. K. Pradhan ◽  
D. H. Coy ◽  
R. T. Jensen
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Maximal Effect ◽  
Dependent Manner ◽  
High Affinity ◽  
Gastric Smooth Muscle ◽  
Guinea Pig Stomach ◽  
Galanin Receptors

Galanin-like immunoactivity occurs in nerves and plexi in muscle layers throughout gastrointestinal tract including the stomach. Galanin can affect gastric emptying and contraction or relaxation of gastric muscle in different species. The aim of this study was to investigate the direct effect of galanin on dispersed gastric smooth muscle cells and to characterize any galanin receptors that mediated any effect. Dispersed gastric smooth muscle cells were prepared from guinea pig stomach by collagenase digestion. Porcine galanin (p-galanin; 1 microM) did not stimulate contraction when present alone; however, p-galanin (1 microM) inhibited carbachol-induced contraction with a half-maximal effect at 7 nM. p-Galanin (1 microM) increased cellular adenosine 3',5'-cyclic monophosphate (cAMP) content by 10 s and caused a maximal increase of 80% over basal. 125I-galanin (porcine) bound to dispersed cells in a time- and temperature-dependent manner. Binding was saturable, reversible, and specific. Binding of 125I-galanin was inhibited almost equally by porcine and rat galanin (Ki = 6-8 nM) but was not inhibited by the galanin-associated peptide [preprogalanin-(108-123)]. The fragment galanin-(1-16) was equally potent to rat galanin; however, the fragment galanin-(9-29) was 56-fold less potent (Ki = 370 nM). Computer analysis demonstrated there were two binding sites for p-galanin on gastric smooth muscle cells, a high-affinity site (Kd = 2.6 nM) with low capacity (Bmax = 175 fmol/mg protein) and a low-affinity site (Kd = 150 nM) with large capacity (Bmax = 3,611 fmol/mg protein).(ABSTRACT TRUNCATED AT 250 WORDS)

Su1539 Mechanisms of PTHrP-induced Suppression of Gastric Smooth Muscle Contractility in the Guinea Pig Stomach

2016 ◽  
Vol 150 (4) ◽  
pp. S521
Author(s):  
Hideomi Ohguchi ◽  
Hikaru Hashitani ◽  
Kenro Imaeda ◽  
Mayo Hachiya ◽  
Eiji Kubota ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Muscle Contractility ◽  
Smooth Muscle Contractility ◽  
Gastric Smooth Muscle ◽  
Guinea Pig Stomach
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