Role of Cell-to-Cell Coupling in Control of Myometrial Contractility and Labor

2019 ◽  
pp. 39-81 ◽  
Author(s):  
Robert E. Garfield
Keyword(s):  
Cell Coupling ◽  
Myometrial Contractility

scholarly journals Role of beta-adrenergic receptor subtypes in pig uterus contractility with inflammation

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Barbara Jana ◽  
Jarosław Całka
Keyword(s):  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Domestic Animals ◽  
Inhibitory Effect ◽  
Receptor Subtypes ◽  
Beta Adrenergic Receptor ◽  
Pharmacological Modulation ◽  
Uterine Inflammation ◽  
Myometrial Contractility

AbstractUterine inflammation is a very common and serious condition in domestic animals. To development and progression of this pathology often lead disturbances in myometrial contractility. Participation of β1-, β2- and β3-adrenergic receptors (ARs) in noradrenaline (NA)-influenced contractility of the pig inflamed uterus was studied. The gilts of SAL- and E.coli-treated groups were administered saline or E.coli suspension into the uterine horns, respectively. Laparotomy was only done in the CON group. Compared to the period before NA administration, this neurotransmitter reduced the tension, amplitude and frequency in uterine strips of the CON and SAL groups. In the E.coli group, NA decreased the amplitude and frequency, and these parameters were lower than in other groups. In the CON, SAL and E.coli groups, β1- and β3-ARs antagonists in more cases did not significantly change and partly eliminated NA inhibitory effect on amplitude and frequency, as compared to NA action alone. In turn, β2-ARs antagonist completely abolished NA relaxatory effect on these parameters in three groups. Summarizing, NA decreases the contractile amplitude and frequency of pig inflamed uterus via all β-ARs subtypes, however, β2-ARs have the greatest importance. Given this, pharmacological modulation of particular β-ARs subtypes can be used to increase inflamed uterus contractility.

Cell coupling in double cones of the fish retina

1985 ◽  
Vol 226 (1243) ◽  
pp. 211-215 ◽  
Keyword(s):  
Intracellular Recording ◽  
Signal Transmission ◽  
Action Spectrum ◽  
Visual Pigments ◽  
Cell Coupling ◽  
Wavelength Detection ◽  
Fish Retina

Isolated double cones containing two distinct visual pigments reveal reciprocal signal transmission between the two cone members. The action spectrum determined by intracellular recording from either of the two members is broader than that in single cones. This suggests a prominent role of double cones in luminosity rather than wavelength detection.

scholarly journals β-Adrenergic receptor stimulation inhibits proarrhythmic alternans in postinfarction border zone cardiomyocytes: a computational analysis

2017 ◽  
Vol 313 (2) ◽  
pp. H338-H353 ◽  
Author(s):  
Jakub Tomek ◽  
Blanca Rodriguez ◽  
Gil Bub ◽  
Jordi Heijman
Keyword(s):  
Adrenergic Receptor ◽  
Border Zone ◽  
Adrenergic Stimulation ◽  
Cell Coupling ◽  
Postmyocardial Infarction ◽  
Model Cell ◽  
Cycle Lengths ◽  
Underlying Mechanisms ◽  
First Time

The border zone (BZ) of the viable myocardium adjacent to an infarct undergoes extensive autonomic and electrical remodeling and is prone to repolarization alternans-induced cardiac arrhythmias. BZ remodeling processes may promote or inhibit Ca2+ and/or repolarization alternans and may differentially affect ventricular arrhythmogenesis. Here, we used a detailed computational model of the canine ventricular cardiomyocyte to study the determinants of alternans in the BZ and their regulation by β-adrenergic receptor (β-AR) stimulation. The BZ model developed Ca2+ transient alternans at slower pacing cycle lengths than the control model, suggesting that the BZ may promote spatially heterogeneous alternans formation in an infarcted heart. β-AR stimulation abolished alternans. By evaluating all combinations of downstream β-AR stimulation targets, we identified both direct (via ryanodine receptor channels) and indirect [via sarcoplasmic reticulum (SR) Ca2+ load] modulation of SR Ca2+ release as critical determinants of Ca2+ transient alternans. These findings were confirmed in a human ventricular cardiomyocyte model. Cell-to-cell coupling indirectly modulated the likelihood of alternans by affecting the action potential upstroke, reducing the trigger for SR Ca2+ release in one-dimensional strand simulations. However, β-AR stimulation inhibited alternans in both single and multicellular simulations. Taken together, these data highlight a potential antiarrhythmic role of sympathetic hyperinnervation in the BZ by reducing the likelihood of alternans and provide new insights into the underlying mechanisms controlling Ca2+ transient and repolarization alternans. NEW & NOTEWORTHY We integrated, for the first time, postmyocardial infarction electrical and autonomic remodeling in a detailed, validated computer model of β-adrenergic stimulation in ventricular cardiomyocytes. Here, we show that β-adrenergic stimulation inhibits alternans and provide novel insights into underlying mechanisms, adding to a recent controversy about pro-/antiarrhythmic effects of postmyocardial infarction hyperinnervation. Listen to this article’s corresponding podcast at http://ajpheart.podbean.com/e/%CE%B2-ar-stimulation-and-alternans-in-border-zone-cardiomyocytes/ .

Role of gap junctions and nitric oxide in control of myometrial contractility

1995 ◽  
Vol 19 (1) ◽  
pp. 41-51 ◽  
Author(s):  
Robert E. Garfield ◽  
Mariam Ali ◽  
Chandrasekhar Yallampalli ◽  
Hidetaka Izumi
Keyword(s):  
Nitric Oxide ◽  
Gap Junctions ◽  
Myometrial Contractility

Role of passive electrical properties during action potential restitution in intact heart

1997 ◽  
Vol 273 (3) ◽  
pp. H1205-H1214 ◽  
Author(s):  
K. R. Laurita ◽  
S. D. Girouard ◽  
Y. Rudy ◽  
D. S. Rosenbaum
Keyword(s):  
Electrical Properties ◽  
Action Potential ◽  
Axial Current ◽  
Propagation Model ◽  
Cell Coupling ◽  
Spatial Gradients ◽  
Dispersion Of Repolarization ◽  
Current Loading ◽  
Passive Electrical Properties

Action potential duration (APD) restitution is classically attributed to membrane ionic currents; however, the role of cell-to-cell coupling in restitution is poorly understood. To test the hypothesis that passive electrical properties of multicellular preparations influence restitution, spatial gradients of transmembrane voltage were measured with high spatial (0.83 mm), voltage (1 mV), and temporal (0.5 ms) resolutions using voltage-sensitive dye in Langendorff-perfused guinea pig ventricle. At short premature coupling intervals, APD failed to shorten in cells located near (< 3 mm) the site of pacing corresponding to the site of earliest repolarization, deviating from classical restitution. In contrast, APD shortened exponentially with increasing stimulus prematurity when pacing was remote from the identical recording site. The mechanism responsible for nonexponential restitution was investigated in a one-dimensional propagation model using the dynamic Luo-Rudy formulation of the ventricular cell and was found to be attributable to depolarizing axial current present in regions of steep repolarization gradients. Moreover, axial current loading attenuated spatial gradients of repolarization that were prominent in the absence of cell-to-cell coupling. These data demonstrate that 1) in contrast to restitution in isolated cells, restitution in multicellular tissue is influenced by axial current from neighboring cells, and 2) in normal myocardium, axial current between cells attenuates dispersion of repolarization during premature stimulation of the heart.

scholarly journals PKA and AKIP1 interact to mediate cAMP-driven COX-2 expression: A potentially pivotal interaction in preterm and term labour

PLoS ONE ◽  
2021 ◽  
Vol 16 (6) ◽  
pp. e0252720
Author(s):  
Angela Yulia ◽  
Natasha Singh ◽  
Alice J. Varley ◽  
Kaiyu Lei ◽  
Danijela Markovic ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Human Myometrium ◽  
Interacting Protein ◽  
Protein Levels ◽  
Early Labour ◽  
Myometrial Contractility ◽  
Cox 2 ◽  
Nuclear Levels ◽  
Term Labour

Previously, we showed that cAMP increased COX-2 expression in myometrial cells via MAPK. Here, we have extended these observations, using primary myometrial cell cultures to show that the cAMP agonist, forskolin, enhances IL-1β-driven COX-2 expression. We then explored the role of A-kinase interacting protein (AKIP1), which modulates the effect of PKA on p65 activation. AKIP1 knockdown reversed the effect of forskolin, such that its addition inhibited IL-1β-induced COX-2 mRNA expression and reduced the IL-1β-induced increase in nuclear levels of p65 and c-jun. Forskolin alone and with IL-1β increased IκBα mRNA expression suggesting that in the context of inflammation and in the presence of AKIP1, cAMP enhances p65 activation. AKIP1 knockdown reversed these changes. Interestingly, AKIP1 knockdown had minimal effect on the ability of forskolin to repress either basal OTR expression or IL-1β-stimulated OTR mRNA expression. AKIP1 was up-regulated by IL-1β, but not stretch and was repressed by cAMP. The mRNA expression of AKIP1 increased in early labour in tandem with an increase in COX-2 mRNA and protein. AKIP1 protein levels were also increased with inflammation and stretch-induced preterm labour. Our results identify a second important cAMP effector-switch occurring at term in human myometrium and suggest that a hitherto unrecognized interaction may exist between AKIP1, NFκB and AP-1. These data add to the proposition that cAMP acts as a key regulator of human myometrial contractility.

Gap junctional communication underpins EDHF-type relaxations evoked by ACh in the rat hepatic artery

2001 ◽  
Vol 280 (6) ◽  
pp. H2441-H2450 ◽  
Author(s):  
Andrew T. Chaytor ◽  
Patricia E. M. Martin ◽  
David H. Edwards ◽  
Tudor M. Griffith
Keyword(s):  
Gap Junctions ◽  
Hepatic Artery ◽  
Lucifer Yellow ◽  
Dye Transfer ◽  
Cell Coupling ◽  
Gap Junctional Communication ◽  
Junctional Communication ◽  
A7r5 Cells ◽  
Gap Junctional

Synthetic peptides homologous to the Gap 26 and Gap 27 domains of the first and second extracellular loops of the major vascular connexins (Cx37, Cx40, and Cx43) have been used to investigate the role of gap junctions in endothelium-derived hyperpolarizing factor (EDHF)-type relaxations of the rat hepatic artery. These peptides were designated 37,40Gap 26,43Gap 26, 37,43Gap 27, and 40Gap 27, according to connexin specificity. When administered at 600 μM, none of the peptides individually affected maximal EDHF-type relaxations to ACh. By contrast, at 300 μM each, paired peptide combinations targeting more than one connexin subtype attenuated relaxation by up to 50%, and responses were abolished by the triple peptide combination 43Gap 26 + 40Gap 27 + 37,43Gap 27. In parallel experiments with A7r5 cells expressing Cx40 and Cx43, neither 43Gap 26 nor40Gap 27 affected intercellular diffusion of Lucifer yellow individually but, in combination, significantly attenuated dye transfer. The findings confirm that functional cell-cell coupling may depend on more than one connexin subtype and demonstrate that direct intercellular communication via gap junctions constructed from Cx37, Cx40, and Cx43 underpins EDHF-type responses in the rat hepatic artery.

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