Role of voltage-dependent potassium channels and myo-endothelial gap junctions in 4-aminopyridine-induced inhibition of acetylcholine relaxation in rat carotid artery

2008 ◽  
Vol 591 (1-3) ◽  
pp. 171-176 ◽  
Author(s):  
Praveen K. Gupta ◽  
Jaganathan Subramani ◽  
Marie Dennis Marcus Leo ◽  
Anurag S. Sikarwar ◽  
Subhashree Parida ◽  
...  
Keyword(s):  
Carotid Artery ◽  
Potassium Channels ◽  
Gap Junctions ◽  
Voltage Dependent

scholarly journals Role of L‐type voltage dependent calcium and large conductance potassium channels in adenosine A 1 receptor mediated vasoconstriction through Cyp4a

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Swati S Kunduri ◽  
Mohammed A Nayeem ◽  
Dovenia S Ponnoth ◽  
Stephen Tilley ◽  
S. Jamal Mustafa
Keyword(s):  
Potassium Channels ◽  
Voltage Dependent

scholarly journals Computational Approaches to Understanding the Role of Fibroblast-Myocyte Interactions in Cardiac Arrhythmogenesis

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Tashalee R. Brown ◽  
Trine Krogh-Madsen ◽  
David J. Christini
Keyword(s):  
Gap Junctions ◽  
Potential Role ◽  
Cardiac Tissue ◽  
Cardiac Fibroblasts ◽  
Cardiac Arrhythmogenesis ◽  
Voltage Dependent ◽  
Underlying Mechanisms ◽  
Slow Propagation

The adult heart is composed of a dense network of cardiomyocytes surrounded by nonmyocytes, the most abundant of which are cardiac fibroblasts. Several cardiac diseases, such as myocardial infarction or dilated cardiomyopathy, are associated with an increased density of fibroblasts, that is, fibrosis. Fibroblasts play a significant role in the development of electrical and mechanical dysfunction of the heart; however the underlying mechanisms are only partially understood. One widely studied mechanism suggests that fibroblasts produce excess extracellular matrix, resulting in collagenous septa. These collagenous septa slow propagation, cause zig-zag conduction paths, and decouple cardiomyocytes resulting in a substrate for arrhythmia. Another emerging mechanism suggests that fibroblasts promote arrhythmogenesis through direct electrical interactions with cardiomyocytes via gap junctions. Due to the challenges of investigating fibroblast-myocyte coupling in native cardiac tissue, computational modeling andin vitroexperiments have facilitated the investigation into the mechanisms underlying fibroblast-mediated changes in cardiomyocyte action potential morphology, conduction velocity, spontaneous excitability, and vulnerability to reentry. In this paper, we summarize the major findings of the existing computational studies investigating the implications of fibroblast-myocyte interactions in the normal and diseased heart. We then present investigations from our group into the potential role of voltage-dependent gap junctions in fibroblast-myocyte interactions.

Enhanced role of potassium channels in relaxations to acetylcholine in hypercholesterolemic rabbit carotid artery

1994 ◽  
Vol 266 (5) ◽  
pp. H2061-H2067 ◽  
Author(s):  
S. Najibi ◽  
C. L. Cowan ◽  
J. J. Palacino ◽  
R. A. Cohen
Keyword(s):  
Nitric Oxide ◽  
Methyl Ester ◽  
Carotid Artery ◽  
Potassium Channels ◽  
Abdominal Aorta ◽  
Combined Treatment ◽  
Rabbit Carotid Artery ◽  
Calcium Dependent ◽  
Endothelium Dependent Relaxation

The effect of hypercholesterolemia for 10 wk on endothelium-dependent relaxations to acetylcholine was studied in isolated rings of rabbit carotid artery and abdominal aorta contracted with phenylephrine or elevated potassium. In these arteries obtained from hypercholesterolemic rabbits, endothelium-dependent relaxations to acetylcholine were not significantly different from those of normal rabbits. In normal and hypercholesterolemic arteries, partial relaxation persisted in the presence of NG-nitro-L-arginine methyl ester (L-NAME), which blocked acetylcholine-induced increases in arterial guanosine 3',5'-cyclic monophosphate (cGMP). Combined treatment with L-NAME and the calcium-dependent potassium-channel inhibitor, charybdotoxin, blocked relaxations in both groups, suggesting that L-NAME-resistant relaxations are mediated by an endothelium-derived hyperpolarizing factor. Charybdotoxin alone or depolarizing potassium had no significant effect on normal carotid artery or normal and hypercholesterolemic abdominal aorta but significantly inhibited relaxations of the carotid artery from cholesterol-fed rabbits. The enhanced role of calcium-dependent potassium channels and the hyperpolarizing factor in relaxation of the hypercholesterolemic carotid artery suggested by these results was likely related to the fact that acetylcholine failed to stimulate cGMP only in that artery. These data suggest that endothelium-dependent relaxation in these rabbit arteries is mediated by nitric oxide-cGMP-dependent and -independent mechanisms. In hypercholesterolemia, the contribution of nitric oxide-cGMP in the carotid artery is reduced, but a hyperpolarizing factor and calcium-dependent potassium channels maintain normal acetylcholine-induced relaxation.

On the physiological role of internodal potassium channels and the security of conduction in myelinated nerve fibres

1984 ◽  
Vol 220 (1221) ◽  
pp. 415-422 ◽  
Keyword(s):  
Electrical Properties ◽  
Potassium Channels ◽  
Theoretical Analysis ◽  
Physiological Role ◽  
Resting Potential ◽  
Nerve Fibres ◽  
Myelinated Nerve ◽  
Voltage Dependent ◽  
Passive Electrical Properties

A theoretical analysis of the passive electrical properties of normal myelinated nerve suggests that the function of the voltage-dependent potassium channels in the internodal axolemma under the myelin sheath is to permit the generation of an internodal resting potential. Calculation shows that if this internodal potential were not present, the nodal potential would be reduced (by electrotonic short-circuiting) thus impairing the security of conduction. This impairment is particularly pronounced with smaller diameter fibres.

Role of the Cilia Membrane in Control of Microtubule Sliding

1980 ◽  
Vol 38 ◽  
pp. 612-615
Author(s):  
Edna S. Kaneshiro
Keyword(s):  
Control Mechanism ◽  
Beat Frequency ◽  
Surface Membrane ◽  
Ciliary Membrane ◽  
Ciliary Beating ◽  
Ciliary Reversal ◽  
Voltage Dependent ◽  
Reversal Mechanism ◽  
And Function

It is currently believed that ciliary beating results from microtubule sliding which is restricted in regions to cause bending. Cilia beat can be modified to bring about changes in beat frequency, cessation of beat and reversal in beat direction. In ciliated protozoans these modifications which determine swimming behavior have been shown to be related to intracellular (intraciliary) Ca2+ concentrations. The Ca2+ levels are in turn governed by the surface ciliary membrane which exhibits increased Ca2+ conductance (permeability) in response to depolarization. Mutants with altered behaviors have been isolated. Pawn mutants fail to exhibit reversal of the effective stroke of ciliary beat and therefore cannot swim backward. They lack the increased inward Ca2+ current in response to depolarizing stimuli. Both normal and pawn Paramecium made leaky to Ca2+ by Triton extrac¬tion of the surface membrane exhibit backward swimming only in reactivating solutions containing greater than IO-6 M Ca2+ Thus in pawns the ciliary reversal mechanism itself is left operational and only the control mechanism at the membrane is affected. The topographic location of voltage-dependent Ca2+ channels has been identified as a component of the ciliary mem¬brane since the inward Ca2+ conductance response is eliminated by deciliation and the return of the response occurs during cilia regeneration. Since the ciliary membrane has been impli¬cated in the control of Ca2+ levels in the cilium and therefore is the site of at least one kind of control of microtubule sliding, we have focused our attention on understanding the structure and function of the membrane.

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