Direct Contractile Response of Isolated Gallbladder Smooth Muscle Cells to Cholecystokinin in Patients with Gallstones

1994 ◽  
Vol 56 (5) ◽  
pp. 434-438 ◽  
Author(s):  
Kazuo Chijiiwa ◽  
Toru Yamasaki ◽  
Yoshiharu Chijiiwa
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Contractile Response ◽  
Muscle Cells

scholarly journals Developmental differences in the contractile response of isolated ovine tracheal smooth muscle cells

2009 ◽  
Vol 44 (6) ◽  
pp. 602-612 ◽  
Author(s):  
Rachel E. Laudadio ◽  
Marla R. Wolfson ◽  
Thomas H. Shaffer ◽  
Steven P. Driska
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Contractile Response ◽  
Muscle Cells ◽  
Developmental Differences ◽  
Tracheal Smooth Muscle

scholarly journals Difference in contractile response of single smooth muscle cells by different determination procedure

1990 ◽  
Vol 52 ◽  
pp. 93
Author(s):  
Yoshimitsu Komatsu ◽  
Yumiko Takemura ◽  
Jun Miyahara ◽  
Toshinori Yamamoto ◽  
Kazutaka Momose
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Contractile Response ◽  
Muscle Cells ◽  
Determination Procedure

Motilin receptors on isolated gastric smooth muscle cells

1988 ◽  
Vol 254 (2) ◽  
pp. G210-G216 ◽  
Author(s):  
D. S. Louie ◽  
C. Owyang
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Smooth Muscle Cells ◽  
Dose Response ◽  
Contractile Response ◽  
Muscle Cells ◽  
Maximal Response ◽  
Gastric Smooth Muscle ◽  
Substance P Antagonist ◽  
Dose Dependent

Motilin has a stimulating effect on gastrointestinal motility. The mechanism of its action is not known. Direct and neuronal effects have been postulated. To determine if receptors are present on smooth muscle cells we investigated the effect of synthetic porcine motilin and its interaction with acetylcholine on isolated guinea pig gastric smooth muscle cells. Motilin elicited a dose-dependent contraction of gastric smooth muscle cells. Minimal (8.3 +/- 1.3%) and maximal (33.9 +/- 2.4%) responses were observed at 10(-12) and 10(-6) M, respectively. The ED50 of motilin was 10(-9) M. Acetylcholine also elicited a dose-response muscle contraction with a maximal response observed at 10(-7) M. Atropine (10(-7) M) completely inhibited the maximal response to acetylcholine but did not have any effect on the contractile response to motilin. In addition, dibutyryl guanosine 3',5'-cyclic monophosphate (10(-3) M) and substance P antagonist, spantide (10(-4) M), also did not inhibit the action of motilin. Acetylcholine (10(-11) M) shifted the dose-response curve of motilin to the left by 1.5 log units. The maximal response to the combination of motilin (10(-6) M) and acetylcholine (10(-11) M) was 32 +/- 3.2%, which was similar to the maximal response to motilin alone. It is concluded that distinct motilin and muscarinic receptors are present on guinea pig gastric smooth muscle cells. The interaction between motilin and acetylcholine is additive and not potentiative.

Effect of hypoxia on the contractile response to KCl, prostaglandin F2α, and hemoglobin

1987 ◽  
Vol 67 (4) ◽  
pp. 565-572 ◽  
Author(s):  
Tadayoshi Nakagomi ◽  
Neal F. Kassell ◽  
Tomio Sasaki ◽  
Shigeru Fujiwara ◽  
R. Michael Lehman ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Contractile Response ◽  
Direct Action ◽  
Cerebral Arteries ◽  
Prostaglandin F2α ◽  
Muscle Cells ◽  
Content Type ◽  
Fine Print

✓ The purpose of this experiment was to evaluate the effect of hypoxia on the in vitro contractile responses of canine basilar artery to KCl, prostaglandin (PG) F2α, and hemoglobin. Hypoxia was induced by changing the bubbling gas mixture in the chamber from 95% O2/5% CO2 to 95% N2/5% CO2. Hypoxia augmented the contractile response developed at 95% O2 to 25 mM and 50 mM KCl, 3 × 10−7 M and 10−5 M PGF2α, and 10−6 M hemoglobin. No significant alteration of the hypoxic augmentation in any preparation exposed to 25 mM KCl, 3 × 10−7 M PGF2α, or 10−6 M hemoglobin was observed with guanethidine (10−5 M), prazosin (10−5 M), methysergide (10−5 M), or diphenhydramine (10−5 M). Endothelial denudation did not affect hypoxic augmentation. Hypoxia did not cause any alteration of the contractile response to 10−6 M PGF2α in Ca++-free media. Pretreatment with a calcium channel blocker, nicardipine, significantly inhibited the hypoxic potentiation of the contractile response to 25 mM KCl, 3 × 10−7 M PGF2α, and 10−6 M hemoglobin. These results suggest that hypoxia augments the contractile response to these agonists by a direct action on the smooth-muscle cells, facilitating the transmembrane influx of extracellular calcium. Hypoxia of smooth-muscle cells in the major cerebral arteries might be involved in the pathogenesis of vasospasm.

Different receptors mediate the action of bombesin-related peptides on gastric smooth muscle cells

1991 ◽  
Vol 260 (5) ◽  
pp. G683-G690 ◽  
Author(s):  
C. Severi ◽  
R. T. Jensen ◽  
V. Erspamer ◽  
L. D'Arpino ◽  
D. H. Coy ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Contractile Response ◽  
Muscle Cells ◽  
Receptor Subtypes ◽  
Gastric Smooth Muscle ◽  
Neuromedin B ◽  
Specific Receptors ◽  
Selective Preservation ◽  
Guinea Pig Stomach

Recent studies suggest that different subtypes of receptors may mediate the action of various bombesin-related peptides in different tissues. In the present study the ability of bombesin and its structurally related peptides [litorin, gastrin-releasing peptide (GRP), GRP18-27, neuromedin B, [Leu8]litorin, and bombesin nonapeptide BN(6-14)] to interact with smooth muscle cells isolated from guinea pig stomach was investigated. Each peptide induced a specific contractile response with potencies (D50 in pM) of [Leu8]litorin (0.7) greater than bombesin (1.2) greater than litorin (3) greater than neuromedin B (3.5) = GRP (3.8) = GRP18-27 (3.9) greater than BN(6-14) (70.9). The specific bombesin receptor antagonist psi 13,14-bombesin differed in its potency for inhibiting equipotent concentrations of bombesin, GRP, or neuromedin B, was equipotent for bombesin or GRP (IC50 12.7 and 22.1 nM), and was 11 times less potent for neuromedin B (IC50 234.5 nM), suggesting the presence of subtypes of receptors mediating the action of bombesin-related peptides. To further investigate this possibility, a technique of receptor protection that enables selective preservation of one receptor type was used. GRP or bombesin protected completely the response to GRP or bombesin but abolished the subsequent contractile response to neuromedin B. Neuromedin B, instead, protected only the response to neuromedin B. These results demonstrate that gastric smooth muscle cells possess specific receptors that interact with bombesin-related peptides and that two receptor subtypes mediate the contractile response to these peptides: one subtype is selective for bombesin or GRP, the other for neuromedin B.

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