scholarly journals The role of the L‐type Ca 2+ channel in refilling functional intracellular Ca 2+ stores in guinea‐pig detrusor smooth muscle

2002 ◽  
Vol 538 (2) ◽  
pp. 357-369 ◽  
Author(s):  
C. Wu ◽  
G. Sui ◽  
C. H. Fry
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Detrusor Smooth Muscle ◽  
Intracellular Ca

Na+/Ca2+ exchange and its role in intracellular Ca2+ regulation in guinea pig detrusor smooth muscle

2001 ◽  
Vol 280 (5) ◽  
pp. C1090-C1096 ◽  
Author(s):  
C. Wu ◽  
C. H. Fry
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Guinea Pig ◽  
Outward Current ◽  
Detrusor Smooth Muscle ◽  
Small Rise ◽  
Intracellular Ca ◽  
Net Flux ◽  
Isolated Smooth Muscle Cells

The role of Na+/Ca2+ exchange in regulating intracellular Ca2+ concentration ([Ca2+]i) in isolated smooth muscle cells from the guinea pig urinary bladder was investigated. Incremental reduction of extracellular Na+ concentration resulted in a graded rise of [Ca2+]i; 50–100 μM strophanthidin also increased [Ca2+]i. A small outward current accompanied the rise of [Ca2+]i in low-Na+ solutions (17.1 ± 1.8 pA in 29.4 mM Na+). The quantity of Ca2+ influx through the exchanger was estimated from the charge carried by the outward current and was ∼30 times that which is necessary to account for the rise of [Ca2+]i, after correction was made for intracellular Ca2+ buffering. Ca2+ influx through the exchanger was able to load intracellular Ca2+ stores. It is concluded that the level of resting [Ca2+]i is not determined by the exchanger, and under resting conditions (membrane potential −50 to −60 mV), there is little net flux through the exchanger. However, a small rise of intracellular Na+ concentration would be sufficient to generate significant net Ca2+ influx.

scholarly journals Role of PTHrP and Sensory Nerve Peptides in Regulating Contractility of Muscularis Mucosae and Detrusor Smooth Muscle in the Guinea Pig Bladder

2016 ◽  
Vol 196 (4) ◽  
pp. 1287-1294 ◽  
Author(s):  
Ken Lee ◽  
Retsu Mitsui ◽  
Shunichi Kajioka ◽  
Seiji Naito ◽  
Hikaru Hashitani
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Sensory Nerve ◽  
Detrusor Smooth Muscle ◽  
Muscularis Mucosae

Role of nitric oxide/cyclic GMP pathway in regulating spontaneous excitations in detrusor smooth muscle of the guinea-pig bladder

2008 ◽  
Vol 27 (5) ◽  
pp. 446-453 ◽  
Author(s):  
Yoshimasa Yanai ◽  
Hikaru Hashitani ◽  
Masa Hayase ◽  
Shoichi Sasaki ◽  
Hikaru Suzuki ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Guinea Pig ◽  
Cyclic Gmp ◽  
Detrusor Smooth Muscle

scholarly journals KV2.1 and electrically silent KV channel subunits control excitability and contractility of guinea pig detrusor smooth muscle

2012 ◽  
Vol 302 (2) ◽  
pp. C360-C372 ◽  
Author(s):  
Kiril L. Hristov ◽  
Muyan Chen ◽  
Rupal P. Soder ◽  
Shankar P. Parajuli ◽  
Qiuping Cheng ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Patch Clamp ◽  
Guinea Pig ◽  
Muscle Tone ◽  
Electrical Field Stimulation ◽  
Resting Membrane Potential ◽  
Detrusor Smooth Muscle ◽  
Kv Channel ◽  
Whole Cell Patch Clamp

Voltage-gated K+ (KV) channels are implicated in detrusor smooth muscle (DSM) function. However, little is known about the functional role of the heterotetrameric KV channels in DSM. In this report, we provide molecular, electrophysiological, and functional evidence for the presence of KV2.1 and electrically silent KV channel subunits in guinea pig DSM. Stromatoxin-1 (ScTx1), a selective inhibitor of the homotetrameric KV2.1, KV2.2, and KV4.2 as well as the heterotetrameric KV2.1/6.3 and KV2.1/9.3 channels, was used to examine the role of these KV channels in DSM function. RT-PCR indicated mRNA expression of KV2.1, KV6.2–6.3, KV8.2, and KV9.1–9.3 subunits in isolated DSM cells. KV2.1 protein expression was confirmed by Western blot and immunocytochemistry. Perforated whole cell patch-clamp experiments revealed that ScTx1 (100 nM) inhibited the amplitude of the KV current in freshly isolated DSM cells. ScTx1 (100 nM) did not significantly change the steady-state activation and inactivation curves for KV current. However, ScTx1 (100 nM) decreased the activation time-constant of the KV current at positive voltages. Although our patch-clamp data could not exclude the presence of the homotetrameric KV2.1 channels, the biophysical characteristics of the ScTx1-sensitive current were consistent with the presence of heterotetrameric KV2.1/silent KV channels. Current-clamp recordings showed that ScTx1 (100 nM) did not change the DSM cell resting membrane potential. ScTx1 (100 nM) increased the spontaneous phasic contraction amplitude, muscle force, and muscle tone as well as the amplitude of the electrical field stimulation-induced contractions of isolated DSM strips. Collectively, our data revealed that KV2.1-containing channels are important physiological regulators of guinea pig DSM excitability and contractility.

Role of capacitative Ca2+ entry in bronchial contraction and remodeling

2002 ◽  
Vol 92 (4) ◽  
pp. 1594-1602 ◽  
Author(s):  
Michele Sweeney ◽  
Sharon S. McDaniel ◽  
Oleksandr Platoshyn ◽  
Shen Zhang ◽  
Ying Yu ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Transient Receptor Potential ◽  
Bronchial Hyperresponsiveness ◽  
Receptor Potential ◽  
Transient Receptor Potential Channel ◽  
Wall Thickening ◽  
Bronchial Wall ◽  
Intracellular Ca ◽  
Transient Receptor

Asthma is characterized by airway inflammation, bronchial hyperresponsiveness, and airway obstruction by bronchospasm and bronchial wall thickening due to smooth muscle hypertrophy. A rise in cytosolic free Ca2+ concentration ([Ca2+]cyt) may serve as a shared signal transduction element that causes bronchial constriction and bronchial wall thickening in asthma. In this study, we examined whether capacitative Ca2+ entry (CCE) induced by depletion of intracellular Ca2+ stores was involved in agonist-mediated bronchial constriction and bronchial smooth muscle cell (BSMC) proliferation. In isolated bronchial rings, acetylcholine (ACh) induced a transient contraction in the absence of extracellular Ca2+ because of Ca2+ release from intracellular Ca2+ stores. Restoration of extracellular Ca2+in the presence of atropine, an M-receptor blocker, induced a further contraction that was apparently caused by a rise in [Ca2+]cyt due to CCE. In single BSMC, amplitudes of the store depletion-activated currents ( I SOC) and CCE were both enhanced when the cells proliferate, whereas chelation of extracellular Ca2+ with EGTA significantly inhibited the cell growth in the presence of serum. Furthermore, the mRNA expression of TRPC1, a transient receptor potential channel gene, was much greater in proliferating BSMC than in growth-arrested cells. Blockade of the store-operated Ca2+channels by Ni2+ decreased I SOC and CCE and markedly attenuated BSMC proliferation. These results suggest that upregulated TRPC1 expression, increased I SOC, enhanced CCE, and elevated [Ca2+]cyt may play important roles in mediating bronchial constriction and BSMC proliferation.

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