Ca2+-induced Ca2+ release activates K+ currents by a cyclic GMP-dependent mechanism in single gastric smooth muscle cells

  title={Ca2+-induced Ca2+ release activates K+ currents by a cyclic GMP-dependent mechanism in single gastric smooth muscle cells},
  author={Dessislava B. Duridanova and Hristo S Gagov and Kiril K. Boev},
  journal={European Journal of Pharmacology},
Thyrotropin-releasing hormone activates KCa channels in gastric smooth muscle cells via intracellular Ca2+ release.
TRH activates K+ channels via inositol-1,4,5-trisphosphate-induced release of Ca2+ in the direction to the plasma membrane, which in turn leads to stimulation of the Ca2-sensitive K+ conductance, membrane hyperpolarization and relaxation.
Ruthenium red-mediated inhibition of large-conductance Ca2+-activated K+ channels in rat pituitary GH3 cells.
Results indicate that ruthenium red can directly suppress the activity of BK(Ca) channels in GH(3) cells, independent on the inhibition of Ca(2+) release from internal stores or mitochondria.
Rebound contraction by nitric oxide in the longitudinal muscle of porcine gastric fundus.
The results suggest that the NO-induced rebound contraction involves both Ca2+-release from the ryanodine-sensitive store and Ca2-influx through L-type channels, and rapid removal of cGMP seems necessary for the rebound contraction.
Pharmacological Modulation of Sarcoplasmic Reticulum Function in Smooth Muscle
An appreciation of the pharmacology and selectivity of agents that interfere with SR function in SM has greatly assisted in unveiling the multifaceted nature of the SR.
Heme oxygenase-2 products activate IKCa: role of CO and iron in guinea pig
It was concluded that CO increases IKCa via its “conventional” signaling pathway, which involves soluble GC and PKG activation and subsequent stimulation of sarcoplasmic reticulum Ca2+ pump activity resulting in Ca2-dependent activation of IK Ca due to the accumulation ofCa2+ into the space near the plasma membrane.
Induction of heme oxygenase in guinea-pig stomach: roles in contraction and in single muscle cell ionic currents.
This is the first study demonstrating that heme oxygenase is an inducible enzyme in guinea-pigs, which exerts a modulatory role on gastric smooth muscle excitability via carbon monoxide production.
Role of constitutively expressed heme oxygenase-2 in the regulation of guinea pig coronary artery tone
Results suggest that the constitutive HO-2 in coronary artery smooth muscle cells plays role in the modulation of tone.
Localised calcium release events in cells from the muscle of guinea‐pig gastric fundus
This study represents the first characterization of localized calcium release events in cells from the gastric fundus, which were novel in their magnitude and kinetic profiles.


Cyclic GMP-induced activation of potassium currents by sarcoplasmic reticulum Ca2+ pump-dependent mechanism.
The authors' data suggest that, in gastric fundus smooth muscles, NO-liberating substances and cGMP analogues contribute to the activation of a Ca2+ -release mechanism from the cell bulk, i.e. the myoplasm surrounding the contractile filaments, towards the plasma membrane, crossing the SR Ca2-stores.
Regulation of intracellular Ca2+ levels in cultured vascular smooth muscle cells. Reduction of Ca2+ by atriopeptin and 8-bromo-cyclic GMP is mediated by cyclic GMP-dependent protein kinase.
It is suggested that repetitively passaged cultured rat aortic smooth muscle cells lose their responsiveness to cGMP concurrently with the loss of cG MP-dependent protein kinase, and restoration of kinase to the cells results in the restoration of responsiveness tocGMP.
Sodium nitroprusside alters Ca2+ flux components and Ca2(+)‐dependent fluxes of K+ and Cl‐ in rat aorta.
NP reduces cytosolic Ca2+, by the combined inhibitory effects on Ca2+ influx and intracellular Ca2- release, and by the stimulation of a Ca2(+)‐ATPase; and the differential sensitivity of the NA and high‐potassium responses to NP may reflect underlying differences inCa2+ handling induced by receptor occupancy and depolarization.
Cytosolic heparin inhibits muscarinic and alpha-adrenergic Ca2+ release in smooth muscle. Physiological role of inositol 1,4,5-trisphosphate in pharmacomechanical coupling.
It is shown that in smooth muscle permeabilized with beta-escin, one of the saponin esters, alpha 1-adrenergic and muscarinic agonists, as well as caffeine and InsP3, cause contractions mediated by Ca2+ release, which supports the conclusion that InsP 3 is the major physiological messenger of the Ca 2+ release component of pharmacomechanical coupling.
Calcium-induced calcium release mechanism in guinea pig taenia caeci
  • M. Iino
  • Biology
    The Journal of general physiology
  • 1989
Rates of the CICR under a physiological ionic milieu were estimated from the results, and a [Ca2+] greater than 1 microM was expected to be necessary for the activation of the Ca release.
Cellular mechanisms regulating [Ca2+]i smooth muscle.
This chapter discusses the Ca2+ transport mechanisms that determine the intracellular Ca 2+ concentration ([Ca2+U]], and thus regulate smooth muscle contraction.
Suppression of steady membrane currents by acetylcholine in single smooth muscle cells of the guinea‐pig gastric fundus.
A major mechanism underlying muscarinic activation is a decrease of a K+ conductance in fundus muscle of the guinea‐pig stomach, and results indicate a suppression of a small Na+ Conductance which is made up by a population of channels that are also blocked by TEA.
Spontaneous sarcoplasmic reticulum calcium release and extrusion from bovine, not porcine, coronary artery smooth muscle.
1. We tested the hypothesis that the Ca(2+)‐loaded sarcoplasmic reticulum (SR) of coronary artery smooth muscle spontaneously releases Ca2+ preferentially toward the sarcolemma to be extruded from