scholarly journals Postsynaptic enhancement by motilin of muscarinic receptor cation currents in duodenal smooth muscle

1998 ◽  
Vol 274 (3) ◽  
pp. G487-G492 ◽  
Author(s):  
Kazunori Yamada ◽  
Hiroe Yanagida ◽  
Yushi Ito ◽  
Ryuji Inoue
Keyword(s):  
Smooth Muscle ◽  
Muscarinic Receptor ◽  
Enzymatic Reactions ◽  
Patch Clamp Technique ◽  
Biochemical Processes ◽  
Cation Current ◽  
Site Of Action ◽  
Cell Variant ◽  
Motilin Receptor

We have investigated a potential role of motilin in amplifying the postsynaptic muscarinic responses in the rabbit duodenal smooth muscle cells, using the whole cell variant of patch-clamp technique. Stimulation of motilin receptors by exogenously applied motilin (1 nM) resulted in a large increase in carbachol (CCh)-induced atropine-sensitive cation current ( ICCh) at threshold concentrations of CCh (0.3–1 μM) at 30°C. This potentiation was abolished in the presence of a specific blocker of motilin receptor (GM109) and was attenuated with increased concentrations of either motilin or CCh, being virtually absent with maximally effective concentrations of these agonists. Motilin failed to potentiate ICChwhen the ambient temperature was reduced to 20°C or if the cation current had been directly activated by internal perfusion with guanosine 5′- O-(3-thiotriphosphate) (50 μM) bypassing the muscarinic receptor. These results suggest that some biochemical processes, such as enzymatic reactions, might be involved in the motilin-induced potentiation and that its site of action might be the muscarinic receptor and/or associated G proteins.

Silver nanoparticles Induce Anti-Proliferative Effects on Airway Smooth Muscle Cells. Role of Nitric Oxide and Muscarinic Receptor Signaling Pathway

2013 ◽  
Vol 65 ◽  
pp. S104
Author(s):  
Manuel Alejandro Ramirez-Lee ◽  
Hector Rosas-Hernandez ◽  
Samuel Salazar-Garcia ◽  
Jose Manuel Gutiérrez-Hernández ◽  
Ricardo Espinosa- Tanguma ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Silver Nanoparticles ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Signaling Pathway ◽  
Muscarinic Receptor ◽  
Airway Smooth Muscle ◽  
Airway Smooth Muscle Cells ◽  
Receptor Signaling Pathway

Preferential potentiation by hypotonic cell swelling of muscarinic cation current in guinea pig ileum

1997 ◽  
Vol 272 (1) ◽  
pp. C240-C253 ◽  
Author(s):  
Y. Waniishi ◽  
R. Inoue ◽  
Y. Ito
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Muscarinic Receptor ◽  
Time Course ◽  
Cell Swelling ◽  
Patch Clamp Technique ◽  
Cationic Current ◽  
Whole Cell Patch Clamp ◽  
Voltage Dependent ◽  
Hypotonic Cell Swelling

The effects of hypotonic cell swelling (HCS) on muscarinic receptor-activated cationic current in guinea pig ileal smooth muscle were investigated by the whole cell patch-clamp technique. With nystatin-perforated recording, reduced external tonicity from 312 to 262 mosM caused cell swelling but hardly affected the membrane currents activated by depolarization, such as outward-rectifying K and voltage-dependent Ca currents. In contrast, the inward current evoked by carbachol at -60 mV was greatly increased (approximately 50%) by the same extent of hypotonicity. This effect is likely to occur through potentiation of nonselective cation channels coupled to the muscarinic receptor (mNSCCs) and probably does not involve elevated intracellular Ca2+ concentration ([Ca2+]i), since neither removal of external Ca2+ nor [Ca2+]i buffering with 10 mM 1,2-bis-(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid significantly affected the results. Furthermore, the time course and degree of this potentiation closely matched those of video-microscopically monitored HCS. These results support the view that mechanosensitive modulation may be a powerful mechanism to regulate mNSCCs activity in gut smooth muscle, together with membrane potential and [Ca2+]i.

Cholinergic control of canine antral immunoreactive gastrin release and motility

1982 ◽  
Vol 60 (7) ◽  
pp. 893-901 ◽  
Author(s):  
J. E. T. Fox ◽  
E. E. Daniel ◽  
J. Jury ◽  
N. S. Track ◽  
S. Chiu
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscarinic Receptor ◽  
Muscle Cell ◽  
Gastrin Release ◽  
Field Stimulation ◽  
Antral Motility ◽  
Stimulation Of ◽  
Extrinsic Nerves

We used acute anaesthetized dogs to investigate the role of cholinergic receptors in the relationship between antral immunoreactive (I) gastrin release and antral motility. Electrical stimulation of extrinsic nerves via the cervical vagus or the nerve of Latarjet appeared to increase I gastrin release and antral motility by separate pathways as blockade of muscarinic receptors, i.e., atropinization inhibited motility but did not alter I gastrin release. On the other hand, blockade of nicotinic receptors by hexamethonium treatment obliterated I gastrin release induced by stimulation of the extrinsic nerves but only reduced motility. Field stimulation of intrinsic nerves via serosal electrodes also increased both I gastrin release and local motility. Since hexamethonium treatment only slightly reduced both I gastrin release and motility and atropinization eliminated both during field stimulation, the presence of a muscarinic receptor in the final pathway for each is proposed.Atropine eliminated carhachol-induced I gastrin release and motility increases, even in the presence of nerve blockade by tetrodotoxin. This suggests that this muscarinic receptor is on the smooth muscle cell itself and possibly on the gastrin cell. However a proposed role of the somatostatin cell in controlling gastrin release is also consistent with these data.Thus, both an intrinsic cholinergic and a separate extrinsic noncholinergic pathway are involved in antral release of I gastrin but initiation of motility appears to involve a final common pathway terminating in a muscarinic receptor on the smooth muscle cell.

scholarly journals Expression and function of KV2-containing channels in human urinary bladder smooth muscle

2012 ◽  
Vol 302 (11) ◽  
pp. C1599-C1608 ◽  
Author(s):  
Kiril L. Hristov ◽  
Muyan Chen ◽  
Serge A. Y. Afeli ◽  
Qiuping Cheng ◽  
Eric S. Rovner ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Patch Clamp ◽  
Electrical Field Stimulation ◽  
Bladder Smooth Muscle ◽  
Rt Pcr ◽  
Patch Clamp Technique ◽  
Whole Cell ◽  
Cell Patch Clamp ◽  
Whole Cell Patch Clamp

The functional role of the voltage-gated K+ (KV) channels in human detrusor smooth muscle (DSM) is largely unexplored. Here, we provide molecular, electrophysiological, and functional evidence for the expression of KV2.1, KV2.2, and the electrically silent KV9.3 subunits in human DSM. Stromatoxin-1 (ScTx1), a selective inhibitor of KV2.1, KV2.2, and KV4.2 homotetrameric channels and of KV2.1/9.3 heterotetrameric channels, was used to examine the role of these channels in human DSM function. Human DSM tissues were obtained during open bladder surgeries from patients without a history of overactive bladder. Freshly isolated human DSM cells were studied using RT-PCR, immunocytochemistry, live-cell Ca2+ imaging, and the perforated whole cell patch-clamp technique. Isometric DSM tension recordings of human DSM isolated strips were conducted using tissue baths. RT-PCR experiments showed mRNA expression of KV2.1, KV2.2, and KV9.3 (but not KV4.2) channel subunits in human isolated DSM cells. KV2.1 and KV2.2 protein expression was confirmed by Western blot analysis and immunocytochemistry. Perforated whole cell patch-clamp experiments revealed that ScTx1 (100 nM) inhibited the amplitude of the voltage step-induced KV current in freshly isolated human DSM cells. ScTx1 (100 nM) significantly increased the intracellular Ca2+ level in DSM cells. In human DSM isolated strips, ScTx1 (100 nM) increased the spontaneous phasic contraction amplitude and muscle force, and enhanced the amplitude of the electrical field stimulation-induced contractions within the range of 3.5–30 Hz stimulation frequencies. These findings reveal that ScTx1-sensitive KV2-containing channels are key regulators of human DSM excitability and contractility and may represent new targets for pharmacological or genetic intervention for bladder dysfunction.

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