Effects of ruthenium red on membrane ionic currents in urinary bladder smooth muscle cells of the guinea-pig

1998 ◽  
Vol 435 (5) ◽  
pp. 645-653 ◽  
Author(s):  
Masaru Hirano ◽  
Y. Imaizumi ◽  
Katsuhiko Muraki ◽  
A. Yamada ◽  
Minoru Watanabe
Keyword(s):  
Smooth Muscle ◽  
Urinary Bladder ◽  
Guinea Pig ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Ionic Currents ◽  
Ruthenium Red ◽  
Bladder Smooth Muscle ◽  
Urinary Bladder Smooth Muscle ◽  
Membrane Ionic Currents

scholarly journals Local Ca2+ coupling between mitochondria and sarcoplasmic reticulum following depolarization in guinea pig urinary bladder smooth muscle cells

2018 ◽  
Vol 314 (1) ◽  
pp. C88-C98 ◽  
Author(s):  
Hisao Yamamura ◽  
Keisuke Kawasaki ◽  
Sou Inagaki ◽  
Yoshiaki Suzuki ◽  
Yuji Imaizumi
Keyword(s):  
Smooth Muscle ◽  
Sarcoplasmic Reticulum ◽  
Urinary Bladder ◽  
Guinea Pig ◽  
Smooth Muscle Cells ◽  
Ryanodine Receptors ◽  
Muscle Cells ◽  
Bladder Smooth Muscle ◽  
Voltage Dependent ◽  
Urinary Bladder Smooth Muscle

Spatiotemporal changes in cytosolic Ca2+ concentration ([Ca2+]c) trigger a number of physiological functions in smooth muscle cells (SMCs). We previously imaged Ca2+-induced Ca2+ release following membrane depolarization as local Ca2+ transients, Ca2+ hotspots, in subplasmalemmal regions. In this study, the physiological significance of mitochondria on local Ca2+ signaling was examined. Cytosolic and mitochondrial Ca2+ images following depolarization or action potentials were recorded in single SMCs from the guinea pig urinary bladder using a fast-scanning confocal fluorescent microscope. Depolarization- and action potential-induced [Ca2+]c transients occurred at several discrete sites in subplasmalemmal regions, peaked within 30 ms, and then spread throughout the whole-cell. In contrast, Ca2+ concentration in the mitochondria matrix ([Ca2+]m) increased after a delay of ~50 ms from the start of depolarization, and then peaked within 500 ms. Following repolarization, [Ca2+]c returned to the resting level with a half-decay time of ~500 ms, while [Ca2+]m recovered more slowly (∼1.5 s). Carbonyl cyanide 4-(trifluoromethoxy)phenylhydrazone, a mitochondrial uncoupler, abolished depolarization-induced [Ca2+]m elevations and slowed [Ca2+]c changes. Importantly, short depolarization-induced changes in [Ca2+]m and transmembrane potential in mitochondria coupled to Ca2+ hotspots were significantly larger than those in other mitochondria. Total internal reflection fluorescence imaging revealed that a subset of mitochondria closely localized with ryanodine receptors and voltage-dependent Ca2+ channels. These results indicate that particular mitochondria are functionally coupled to ion channels and sarcoplasmic reticulum fragments within the local Ca2+ microdomain, and thus, strongly contribute to [Ca2+]c regulation in SMCs.

scholarly journals Stretch-induced Calcium Release in Smooth Muscle

2002 ◽  
Vol 119 (6) ◽  
pp. 533-543 ◽  
Author(s):  
Guangju Ji ◽  
Robert J. Barsotti ◽  
Morris E. Feldman ◽  
Michael I. Kotlikoff
Keyword(s):  
Smooth Muscle ◽  
Urinary Bladder ◽  
Smooth Muscle Cells ◽  
Calcium Release ◽  
Muscle Cells ◽  
Intraluminal Pressure ◽  
Bladder Smooth Muscle ◽  
Urinary Bladder Smooth Muscle ◽  
Inward Currents ◽  
Longitudinal Stretch

Smooth muscle cells undergo substantial increases in length, passively stretching during increases in intraluminal pressure in vessels and hollow organs. Active contractile responses to counteract increased transmural pressure were first described almost a century ago (Bayliss, 1902) and several mechanisms have been advanced to explain this phenomenon. We report here that elongation of smooth muscle cells results in ryanodine receptor–mediated Ca2+ release in individual myocytes. Mechanical elongation of isolated, single urinary bladder myocytes to ∼120% of slack length (ΔL = 20) evoked Ca2+ release from intracellular stores in the form of single Ca2+ sparks and propagated Ca2+ waves. Ca2+ release was not due to calcium-induced calcium release, as release was observed in Ca2+-free extracellular solution and when free Ca2+ ions in the cytosol were strongly buffered to prevent increases in [Ca2+]i. Stretch-induced calcium release (SICR) was not affected by inhibition of InsP3R-mediated Ca2+ release, but was completely blocked by ryanodine. Release occurred in the absence of previously reported stretch-activated currents; however, SICR evoked calcium-activated chloride currents in the form of transient inward currents, suggesting a regulatory mechanism for the generation of spontaneous currents in smooth muscle. SICR was also observed in individual myocytes during stretch of intact urinary bladder smooth muscle segments. Thus, longitudinal stretch of smooth muscle cells induces Ca2+ release through gating of RYR. SICR may be an important component of the physiological response to increases in luminal pressure in smooth muscle tissues.

scholarly journals SK4 Encodes Intermediate Conductance Ca2+-Activated K+ Channels in Mouse Urinary Bladder Smooth Muscle Cells

2000 ◽  
Vol 84 (1) ◽  
pp. 97-100 ◽  
Author(s):  
Susumu Ohya ◽  
Shunichi Kimura ◽  
Mika Kitsukawa ◽  
Katsuhiko Muraki ◽  
Minoru Watanabe ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Urinary Bladder ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Bladder Smooth Muscle ◽  
K Channels ◽  
Urinary Bladder Smooth Muscle

scholarly journals Induction of Smooth Muscle Cell-Like Phenotype in Marrow-Derived Cells among Regenerating Urinary Bladder Smooth Muscle Cells

2005 ◽  
Vol 166 (2) ◽  
pp. 565-573 ◽  
Author(s):  
Akihiro Kanematsu ◽  
Shingo Yamamoto ◽  
Eri Iwai-Kanai ◽  
Isao Kanatani ◽  
Masaaki Imamura ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Urinary Bladder ◽  
Smooth Muscle Cells ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Muscle Cells ◽  
Bladder Smooth Muscle ◽  
Urinary Bladder Smooth Muscle
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