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Excitation-Contraction Coupling in Ureteric Smooth Muscle: Mechanisms Driving Ureteric Peristalsis

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Smooth Muscle Spontaneous Activity

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 1124))

Abstract

The ureter acts as a functional syncytium and is controlled by a propagating plateau-type action potential (AP) which gives rise to a wave of contraction (ureteral peristalsis) via a process called excitation-contraction (E-C)coupling. The second messenger Ca2+ activates Ca2+/calmodulin-dependent myosin light chain kinase-dependent phosphorylation of 20-kDa regulatory light chains of myosin which leads to ureteric contraction. Ca2+ entry from the extracellular space via voltage-gated L-type Ca2+ channels (VGCCs) provides the major source of activator Ca2+, responsible for generation of both the AP and a Ca2+ transient that appears as an intercellular Ca2+ wave. The AP, inward Ca2+ current, Ca2+ transient and twitch contraction are all fully blocked by the selective L-type Ca2+ channel blocker nifedipine. Ca2+ entry via VGCCs, coupled to activation of Ca2+-sensitive K+ (KCa) or Cl− (ClCa) channels, acts as a negative or positive feedback mechanism, respectively, to control excitability and the amplitude and duration of the plateau component of the AP, Ca2+ transient and twitch contraction. The ureter, isolated from the pelvis, is not spontaneously active. However, spontaneous activity can be initiated in the proximal and distal ureter by a variety of biological effectors such as neurotransmitters, paracrine, endocrine and inflammatory factors. Applied agonists depolarise ureteric smooth muscles cells to threshold of AP activation, initiating propagating intercellular AP-mediated Ca2+ waves to produce antegrade and/or retrograde ureteric peristalsis. Several mechanisms have been proposed to describe agonist-induced depolarization of ureteric smooth muscle, which include suppression of K+ channels, stimulation of ClCa current and activation of non-selective cation receptor/store operated channels.

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Authors and Affiliations

  1. Department of Cellular and Molecular Physiology, Institute of Translational Medicine, University of Liverpool, Liverpool, UK

    Theodor Burdyga

  2. School of Biomedical Sciences, Faculty of Medicine, Nursing and Health Sciences, Monash University, Clayton, VIC, Australia

    Richard J. Lang

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  1. Theodor Burdyga
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Correspondence to Theodor Burdyga .

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Editors and Affiliations

  1. Nagoya City University, Nagoya, Aichi, Japan

    Hikaru Hashitani

  2. Monash University, Melbourne, VIC, Australia

    Richard J. Lang

1 Electronic Supplementary Material

Propagating intercellular Ca2+ waves in the upper and lower segments of the guinea pig ureter. See Fig. 4.4 and text for details (MPG 2270 kb)

Effects of low concentration of Caffeine (1 mM) on Ca2+ signalling of isolated guinea pig ureteric myocytes. See Fig. 4.5 and text for details (MPG 728 kb)

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Burdyga, T., Lang, R.J. (2019). Excitation-Contraction Coupling in Ureteric Smooth Muscle: Mechanisms Driving Ureteric Peristalsis. In: Hashitani, H., Lang, R. (eds) Smooth Muscle Spontaneous Activity. Advances in Experimental Medicine and Biology, vol 1124. Springer, Singapore. https://doi.org/10.1007/978-981-13-5895-1_4

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