ArticleThe Journal of physiology2007
Ryanodine receptor type 2 deficiency changes excitation-contraction coupling and membrane potential in urinary bladder smooth muscle.
Article in The Journal of physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 42 citations in OpenAlex.
- Cells and ionic conductances contributing to spontaneous activity in bladder and urethral smooth muscle.The Journal of physiology · 2026Review
- Smooth muscle of the lower urinary tract: BK-RyR coupling in physiology and pathophysiology.Journal of muscle research and cell motility · 2025Review
- Structure, Function, and Regulation of the Junctophilin Family.Annual review of physiology · 2024Review
- Importance of Spatial Arrangement of Cardiomyocyte Network for Precise and Stable On-Chip Predictive Cardiotoxicity Measurement.Micromachines · 2023Article
- Igniting CaProceedings of the National Academy of Sciences of the United States of America · 2020Article
- The intracellular CaProceedings of the National Academy of Sciences of the United States of America · 2020Article
- Reduced CaAging · 2020Article
- Ryanodine receptor type 3 does not contribute to contractions in the mouse myometrium regardless of pregnancy.Pflugers Archiv : European journal of physiology · 2017Article
- Big-conductance CaChannels (Austin, Tex.) · 2016Review
- Chronic fetal exposure to caffeine altered resistance vessel functions via RyRs-BKCa down-regulation in rat offspring.Scientific reports · 2015Article
- Functional link between muscarinic receptors and large-conductance Ca2+ -activated K+ channels in freshly isolated human detrusor smooth muscle cells.Pflugers Archiv : European journal of physiology · 2015Article
- Central role of the BK channel in urinary bladder smooth muscle physiology and pathophysiology.American journal of physiology. Regulatory, integrative and comparative physiology · 2014Review
- Facilitated hyperpolarization signaling in vascular smooth muscle-overexpressing TRIC-A channels.The Journal of biological chemistry · 2013Article
- Selective inhibition of phosphodiesterase 1 relaxes urinary bladder smooth muscle: role for ryanodine receptor-mediated BK channel activation.American journal of physiology. Cell physiology · 2012Article
- Inhibition of phosphodiesterases relaxes detrusor smooth muscle via activation of the large-conductance voltage- and Ca²⁺-activated K⁺ channel.American journal of physiology. Cell physiology · 2012Article
- Role of potassium ion channels in detrusor smooth muscle function and dysfunction.Nature reviews. Urology · 2011Review
- Ryanodine receptor studies using genetically engineered mice.FEBS letters · 2010Review
- Membrane depolarization causes a direct activation of G protein-coupled receptors leading to local Ca2+ release in smooth muscle.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Genetic evidence for functional role of ryanodine receptor 1 in pulmonary artery smooth muscle cells.Pflugers Archiv : European journal of physiology · 2009Article
- Role of ryanodine receptor subtypes in initiation and formation of calcium sparks in arterial smooth muscle: comparison with striated muscle.Journal of biomedicine & biotechnology · 2009Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The possibility that the ryanodine receptor type 2 (RyR2) can function as the major Ca(2+)-induced Ca(2+) release (CICR) channel in excitation-contraction (E-C) coupling was examined in smooth muscle cells (SMCs) isolated from urinary bladder (UB) of RyR2 heterozygous KO mice (RyR2+/-). RyR2 mRNA expression in UB from RyR2+/- was much lower than that in wild-type (RyR2+/+. In single UBSMCs from RyR2+/+, membrane depolarization under voltage clamp initially induced several local Ca(2+) transients (hot spots) in peripheral areas of the cell. Then, Ca(2+) waves spread from Ca(2+) hot spots to other areas of the myocyte. The number of Ca(2+) hot spots elicited by a short depolarization (< 20 ms) in UBSMCs of RyR2+/- was significantly smaller than in those of RyR2+/+. The force development induced either by direct electrical stimulation or by 10 microm acetylcholine in tissue segments of RyR2+/- was smaller than and comparable to those in RyR2+/+, respectively. The frequency of spontaneous transient outward currents in single myocytes and the membrane depolarization by 1 microm paxilline in tissue segments from RyR2+/- were significantly lower and smaller than those in RyR2+/+, respectively. The urination frequency and volume per voiding in RyR2+/- were significantly increased and reduced, respectively, compared with RyR2+/+. In conclusion, RyR2 plays a crucial role in the regulation of CICR during E-C coupling and also in the regulation of resting membrane potential, presumably via the modulation of Ca(2+)-dependent K(+) channel activity in UBSMCs and, thereby, has a pivotal role in the control of bladder activity.
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