EXCITATION-CONTRACTION COUPLING IN GASTROINTESTINAL AND OTHER SMOOTH MUSCLES

• T. B. Bolton

  Department of Pharmacology and Clinical Pharmacology, St George's Hospital Medical School, London SW17 0RE, United Kingdom;

• S. A. Prestwich

  Department of Pharmacology and Clinical Pharmacology, St George's Hospital Medical School, London SW17 0RE, United Kingdom;

• A. V. Zholos

  Department of Pharmacology and Clinical Pharmacology, St George's Hospital Medical School, London SW17 0RE, United Kingdom;

• D. V. Gordienko

  Department of Pharmacology and Clinical Pharmacology, St George's Hospital Medical School, London SW17 0RE, United Kingdom;

Abstract

▪ Abstract  The main contributors to increases in [Ca 2+ ] i and tension are the entry of Ca 2+ through voltage-dependent channels opened by depolarization or during action potential (AP) or slow-wave discharge, and Ca 2+ release from store sites in the cell by the action of IP 3 or by Ca 2+ -induced Ca 2+ -release (CICR). The entry of Ca 2+ during an AP triggers CICR from up to 20 or more subplasmalemmal store sites (seen as hot spots, using fluorescent indicators); Ca 2+ waves then spread from these hot spots, which results in a rise in [Ca 2+ ] i throughout the cell. Spontaneous transient releases of store Ca 2+ , previously detected as spontaneous transient outward currents (STOCs), are seen as sparks when fluorescent indicators are used. Sparks occur at certain preferred locations—frequent discharge sites (FDSs)—and these and hot spots may represent aggregations of sarcoplasmic reticulum scattered throughout the cytoplasm. Activation of receptors for excitatory signal molecules generally depolarizes the cell while it increases the production of IP 3 (causing calcium store release) and diacylglycerols (which activate protein kinases). Activation of receptors for inhibitory signal molecules increases the activity of protein kinases through increases in cAMP or cGMP and often hyperpolarizes the cell. Other receptors link to tyrosine kinases, which trigger signal cascades interacting with trimeric G-protein systems.

Journal

• Annual Review of Physiology

  Annual Review of Physiology 61 (1), 85-115, 1999-03

  Annual Reviews

Keywords

• Physiology

Details

• CRID: 1364233269272273280
• NII Article ID: 30022153654
• DOI: 10.1146/annurev.physiol.61.1.85
• ISSN: 15451585
• ISSN: 00664278
• Web Site: https://www.annualreviews.org/doi/pdf/10.1146/annurev.physiol.61.1.85
• Data Source:
  • Crossref
  • CiNii Articles