ArticleBritish journal of pharmacology2010
Role of mitochondria in contraction and pacemaking in the mouse uterus.
Article in British journal of pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 25 citations in OpenAlex.
- Assessing Tocolytic Potency: Variability and Accuracy of AUC Versus Amplitude-Based Assessment of Pregnant Human Myometrial Contractions Ex Vivo.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- Shaping the waves: Mitochondrial regulation of calcium oscillations in smooth muscle.The Journal of physiology · 2025Article
- Assessing the Potency of the Novel Tocolytics 2-APB, Glycyl-H-1152, and HC-067047 in Pregnant Human Myometrium.Reproductive sciences (Thousand Oaks, Calif.) · 2023Article
- Blocking the BKCa channel induces NF-κB nuclear translocation by increasing nuclear calcium concentration†.Biology of reproduction · 2022Article
- Uterine contractions in rodent models and humans.Acta physiologica (Oxford, England) · 2021Review
- Effect of reproductive ageing on pregnant mouse uterus and cervix.The Journal of physiology · 2017Article
- BKCa channel regulates calcium oscillations induced by alpha-2-macroglobulin in human myometrial smooth muscle cells.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Store-operated Ca²⁺ entry and depolarization explain the anomalous behaviour of myometrial SR: effects of SERCA inhibition on electrical activity, Ca²⁺ and force.Cell calcium · 2014Article
- Phasic contractions of the mouse vagina and cervix at different phases of the estrus cycle and during late pregnancy.PloS one · 2014Article
- Functional insights into modulation of BKCa channel activity to alter myometrial contractility.Frontiers in physiology · 2014Review
- Telocytes: ultrastructural, immunohistochemical and electrophysiological characteristics in human myometrium.Reproduction (Cambridge, England) · 2013Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeUterine spontaneous contraction and pacemaking are poorly understood. This study investigates the role of the mitochondrial Ca(2+) store in uterine activity. EXPERIMENTAL APPROACH: We investigated the effects of mitochondrial and sarco-endoplasmic reticulum (SER) inhibitors on contraction, membrane potential (Vm) and cytosolic Ca(2+) concentration ([Ca(2+) ](c) ) in longitudinal smooth muscle of the mouse uterus. KEY
resultsThe mitochondrial agents rotenone, carbonylcyanide-3-chlorophenylhydrazone (CCCP), 7-chloro-5-(2-chlorophenyl)-1,5-dihydro-4,1-benzothiazepin-2(3H)-one (CGP37157) and kaempferol decreased the force of contractions. The ATP synthase inhibitor oligomycin had no significant effect. The effects of these agents were compared with those of SER inhibitors cyclopiazonic acid (CPA), 2-amino ethoxyphenylborate (2-APB) and caffeine. All agents, except CPA and oligomycin, decreased contractile force. CPA and CCCP transiently increased contraction frequency, which returned to control levels, whereas rotenone, CGP37157, kaempferol and 2-APB decreased frequency and caffeine had no significant effect. Application of the mitochondrial agents when CPA functionally inhibited stores did not change contraction frequency but, with the exception of kaempferol, decreased force. CCCP caused depolarization and maintained increase in [Ca(2+) ](c) or depolarization/transient hyperpolarization and transient increase in [Ca(2+) ](c) for oestrus and di-oestrus tissues respectively. Rotenone caused hyperpolarization and maintained increase in [Ca(2+) ](c) . CGP37157 and kaempferol caused hyperpolarization but no measurable change in [Ca(2+) ](c) . Application of a range of K(+) channel blockers indicated a role of Ca(2+) -activated K(+) (K(Ca) ) channels in the CCCP- and CGP37157-induced actions. CONCLUSIONS AND IMPLICATIONS: Mitochondria have a modulatory role on uterine contractions, with mitochondrial inhibition reducing contraction amplitude and pacemaker frequency by changes in Vm, [Ca(2+) ](c) and/or Ca(2+) influx.
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