ArticleThe Journal of physiology2004
Rho-kinase inhibition and electromechanical coupling in rat and guinea-pig ureter smooth muscle: Ca2+-dependent and -independent mechanisms.
Article in The Journal of physiology, 2004. 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, 68 citations in OpenAlex.
- The Rho-kinase inhibitor Y27632 promotes ureteral relaxation in an in vivo rat model for partial ureteral obstruction.World journal of urology · 2023Article
- Vascular mechanotransduction.Physiological reviews · 2023Review
- KAmerican journal of physiology. Cell physiology · 2022Review
- Ups and downs of calcium in the heart.The Journal of physiology · 2018Article
- Chemerin-induced arterial contraction is GVascular pharmacology · 2017Article
- Role of endothelin-1 for the regulation of renal pelvic function.Pflugers Archiv : European journal of physiology · 2016Article
- The effects of Ginseng Java root extract on uterine contractility in nonpregnant rats.Physiological reports · 2014Article
- 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
- Abnormal tracheal smooth muscle function in the CF mouse.Physiological reports · 2013Article
- Role of PKC and RhoA/ROCK pathways in the spontaneous phasic activity in the rectal smooth muscle.American journal of physiology. Gastrointestinal and liver physiology · 2013Article
- Oxidized LDL/CD36 interaction induces loss of cell polarity and inhibits macrophage locomotion.Molecular biology of the cell · 2012Article
- The importance of Rho-associated kinase-induced Ca2+ sensitization as a component of electromechanical and pharmacomechanical coupling in rat ureteric smooth muscle.Cell calcium · 2011Article
- Endothelin-1-induced activation of rat renal pelvic contractions depends on cyclooxygenase-1 and Rho kinase.American journal of physiology. Regulatory, integrative and comparative physiology · 2010Article
- Rho kinase and protein kinase C involvement in vascular smooth muscle myofilament calcium sensitization in arteries from diabetic rats.British journal of pharmacology · 2010Article
- Ca2+ sensitization via phosphorylation of myosin phosphatase targeting subunit at threonine-855 by Rho kinase contributes to the arterial myogenic response.The Journal of physiology · 2009Article
- A novel videomicroscopic technique for studying rat ureteral peristalsis in vivo.World journal of urology · 2009Article
- Role of protein kinase Czeta and calcium entry in KCl-induced vascular smooth muscle calcium sensitization and feedback control of cellular calcium levels.The Journal of pharmacology and experimental therapeutics · 2009Article
- Myosin light chain kinase is central to smooth muscle contraction and required for gastrointestinal motility in mice.Gastroenterology · 2008Article
- Myosin light chain kinase activation and calcium sensitization in smooth muscle in vivo.American journal of physiology. Cell physiology · 2008Article
- Calyculin A, an enhancer of myosin, speeds up anaphase chromosome movement.Cell & chromosome · 2007Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent data have shown Ca(2+)-dependent activation of Rho-kinase by sustained depolarization of arterial smooth muscle. Visceral smooth muscles, however, contract phasically in response to action potentials and it is unclear whether Ca(2+)-dependent or -independent Rho-kinase activation occurs. We have therefore investigated this, under physiologically relevant conditions, in intact ureter. Action potentials, ionic currents, Ca(2+) transients, myosin light chain (MLC) phosphorylation and phasic contraction evoked by action potentials in guinea-pig and rat ureter were investigated. In rat, but not guinea-pig ureter, three Rho-kinase inhibitors, Y-27632, HA-1077 and H-1152, significantly decreased phasic contractions and Ca(2+) transients. Voltage- and current-clamp data showed that Rho-kinase inhibition reduced the plateau component of the action potential, inhibited Ca(2+)-channels and, indirectly, Ca(2+)-activated Cl(-) channels. The Ca(2+) channel agonist Bay K8644 could reverse these effects. The K(+) channel blocker TEA could also reverse the inhibitory effect of Y-27632 on the action potential and Ca(2+) transient. Ca(2+) transients and inward current, activated by carbachol-induced sarcoplasmic reticulum Ca(2+)release, were not affected by Rho-kinase inhibition. Rho-kinase inhibition produced a Ca(2+)-independent increase in the relaxation rate of contraction, associated with acceleration of MLC dephosphorylation, which was sensitive to calyculin A. These data show for the first time that: (1) Rho-kinase has major effects on Ca(2+) signalling associated with the action potential, (2) this effect is species dependent and (3) Rho-kinase controls relaxation of phasic contraction of myogenic origin. Thus Rho-kinase can modulate phasic smooth muscle in the absence of agonist, and the mechanisms are both Ca(2+)-dependent, involving ion channels, and Ca(2+)-independent, involving MLC phosphorylation activity.
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