scholarly journals Smooth muscle membrane potential modulates endothelium‐dependent relaxation of rat basilar artery via myo‐endothelial gap junctions

2002 ◽  
Vol 545 (3) ◽  
pp. 975-986 ◽  
Author(s):  
Tracy Allen ◽  
Mircea Iftinca ◽  
William C. Cole ◽  
Frances Plane
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Gap Junctions ◽  
Basilar Artery ◽  
Muscle Membrane ◽  
Smooth Muscle Membrane ◽  
Endothelium Dependent Relaxation

Effects of bethanechol and the octapeptide of cholecystokinin on colonic smooth muscle in the cat

1987 ◽  
Vol 252 (5) ◽  
pp. G654-G661
Author(s):  
W. J. Snape ◽  
S. T. Tan ◽  
H. W. Kao
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Slow Wave ◽  
Spike Activity ◽  
Membrane Resistance ◽  
Wave Pattern ◽  
Isometric Tension ◽  
Muscle Membrane ◽  
Maximum Effect ◽  
Smooth Muscle Membrane

The aim of this study is to compare the action of the cholinergic agonist, bethanechol, with the action of the octapeptide of cholecystokinin (CCK-OP) on feline circular colonic smooth muscle membrane potential and isometric tension, using the double sucrose gap. Depolarization of the membrane greater than 10 mV by K+ or bethanechol increased tension and spontaneous spike activity. CCK-OP (10(-9) M) depolarized the membrane (6.1 +/- 1.3 mV) without an increase in tension or spike activity. Depolarization of the membrane by increasing [K+]o was associated with a decrease in the membrane resistance. The slow-wave duration (2.3 +/- 0.2 s) was unchanged by administration of K+ or bethanechol but was prolonged after increasing concentrations of CCK-OP. The maximum effect occurred at a 10(-10) M concentration of CCK-OP (4.5 +/- 0.4 s, P less than 0.01). At higher concentrations of CCK-OP (greater than 10(-10) M), the slow-wave pattern became disorganized. Addition of increasing concentrations of [K+]o or bethanechol, but not CCK-OP, stimulated a concentration-dependent increase in the maximum rate of rise (dV/dtmax) of an evoked spike potential. These studies suggest 1) bethanechol decreased the membrane potential without altering the slow-wave activity, whereas CCK-OP has a minimal effect on the membrane potential but distorted the slow-wave shape; 2) an increased amplitude of the spike and dV/dtmax of the spike were associated with an increase in phasic contractions after bethanechol or increased [K+]o; 3) the lack of an increase in the spike amplitude and the dV/dtmax to CCK-OP was associated with no increase in phasic contraction.

KCa-channel blockade prevents sustained pressure-induced depolarization in rat mesenteric small arteries

1997 ◽  
Vol 272 (5) ◽  
pp. H2241-H2249 ◽  
Author(s):  
J. P. Wesselman ◽  
R. Schubert ◽  
E. D. VanBavel ◽  
H. Nilsson ◽  
M. J. Mulvany
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Transmural Pressure ◽  
Muscle Membrane ◽  
Outer Diameter ◽  
Small Arteries ◽  
Pressure Elevation ◽  
Kca Channels ◽  
Smooth Muscle Membrane

In small blood vessels, elevation of transmural pressure induces myogenic constrictions and smooth muscle depolarization. The role of calcium-activated K+ channels (KCa channels) in these responses was examined in cannulated rat mesenteric small arteries. Inner and outer diameter were continuously monitored with a video technique. Smooth muscle membrane potential was recorded simultaneously using microelectrodes. To test for myogenic responsiveness, the transmural pressure was changed stepwise in the range between 10 and 120 mmHg. Pressure elevation induced moderate myogenic responses and significant depolarization, from -54.5 +/- 0.4 (SE) mV (n = 56) at 10 mmHg to -47.3 +/- 1.8 mV (n = 12) at 120 mmHg. Norepinephrine (NE, 0.67 and 10 microM) induced constriction and vasomotion, augmented myogenic responsiveness, and shifted the pressure-membrane potential relation to more depolarized values. Blockade of the Kca channels with charybdotoxin (ChTX) suppressed the responsiveness to pressure. In the absence of ChTX, with 0.67 microM NE, pressure elevation from 10 to 120 mmHg induced depolarization from -46.9 +/- 1.0 (n = 16) to -35.8 +/- 0.7 (n = 12) mV, whereas because of the myogenic response, the diameter increased only by 7%. In the presence of ChTX, with 0.3 microM NE, pressure changed the membrane potential from -41.0 +/- 1.1 (n = 12) to -37.8 +/- 0.7 mV (n = 4), which was not significant, and the diameter increased by 28%. These results demonstrate that blockade of KCa channels reduces responsiveness to pressure elevation. This suggests that pressure may induce depolarization and concomitant myogenic responsiveness by closure of KCa channels.

Physiological roles and properties of potassium channels in arterial smooth muscle

1995 ◽  
Vol 268 (4) ◽  
pp. C799-C822 ◽  
Author(s):  
M. T. Nelson ◽  
J. M. Quayle
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Smooth Muscle Cells ◽  
Katp Channels ◽  
Muscle Cells ◽  
Muscle Membrane ◽  
K Channel ◽  
Arterial Smooth Muscle ◽  
K Channels ◽  
Smooth Muscle Membrane

This review examines the properties and roles of the four types of K+ channels that have been identified in the cell membrane of arterial smooth muscle cells. 1) Voltage-dependent K+ (KV) channels increase their activity with membrane depolarization and are important regulators of smooth muscle membrane potential in response to depolarizing stimuli. 2) Ca(2+)-activated K+ (KCa) channels respond to changes in intracellular Ca2+ to regulate membrane potential and play an important role in the control of myogenic tone in small arteries. 3) Inward rectifier K+ (KIR) channels regulate membrane potential in smooth muscle cells from several types of resistance arteries and may be responsible for external K(+)-induced dilations. 4) ATP-sensitive K+ (KATP) channels respond to changes in cellular metabolism and are targets of a variety of vasodilating stimuli. The main conclusions of this review are: 1) regulation of arterial smooth muscle membrane potential through activation or inhibition of K+ channel activity provides an important mechanism to dilate or constrict arteries; 2) KV, KCa, KIR, and KATP channels serve unique functions in the regulation of arterial smooth muscle membrane potential; and 3) K+ channels integrate a variety of vasoactive signals to dilate or constrict arteries through regulation of the membrane potential in arterial smooth muscle.

scholarly journals Endothelial coordination of cerebral vasomotion via myoendothelial gap junctions containing connexins 37 and 40

2006 ◽  
Vol 291 (5) ◽  
pp. H2047-H2056 ◽  
Author(s):  
Rebecca E. Haddock ◽  
T. Hilton Grayson ◽  
Therese D. Brackenbury ◽  
Kate R. Meaney ◽  
Craig B. Neylon ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Endothelial Cell ◽  
Gap Junctions ◽  
Basilar Artery ◽  
Electrical Coupling ◽  
Potential Oscillations ◽  
Membrane Potential Oscillations ◽  
Rhythmical Contractions ◽  
Conventional Electron Microscopy

Control of cerebral vasculature differs from that of systemic vessels outside the blood-brain barrier. The hypothesis that the endothelium modulates vasomotion via direct myoendothelial coupling was investigated in a small vessel of the cerebral circulation. In the primary branch of the rat basilar artery, membrane potential, diameter, and calcium dynamics associated with vasomotion were examined using selective inhibitors of endothelial function in intact and endothelium-denuded arteries. Vessel anatomy, protein, and mRNA expression were studied using conventional electron microscopy high-resolution ultrastructural and confocal immunohistochemistry and quantitative PCR. Membrane potential oscillations were present in both endothelial cells and smooth muscle cells (SMCs), and these preceded rhythmical contractions during which adjacent SMC intracellular calcium concentration ([Ca2+]i) waves were synchronized. Endothelium removal abolished vasomotion and desynchronized adjacent smooth muscle cell [Ca2+]i waves. NG-nitro-l-arginine methyl ester (10 μM) did not mimic this effect, and dibutyryl cGMP (300 μM) failed to resynchronize [Ca2+]i waves in endothelium-denuded arteries. Combined charybdotoxin and apamin abolished vasomotion and depolarized and constricted vessels, even in absence of endothelium. Separately, 37,43Gap27 and 40Gap27 abolished vasomotion. Extensive myoendothelial gap junctions (3 per endothelial cell) composed of connexins 37 and 40 connected the endothelial cell and SMC layers. Synchronized vasomotion in rat basilar artery is endothelium dependent, with [Ca2+]i waves generated within SMCs being coordinated by electrical coupling via myoendothelial gap junctions.

scholarly journals Extracellular Cl−regulates electrical slow waves and setting of smooth muscle membrane potential by interstitial cells of Cajal in mouse jejunum

2017 ◽  
Vol 103 (1) ◽  
pp. 40-57 ◽  
Author(s):  
Siva Arumugam Saravanaperumal ◽  
Simon J. Gibbons ◽  
John Malysz ◽  
Lei Sha ◽  
David R. Linden ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Interstitial Cells Of Cajal ◽  
Interstitial Cells ◽  
Slow Waves ◽  
Muscle Membrane ◽  
Smooth Muscle Membrane ◽  
Cells Of Cajal

The relation between the structure and innervation of small arteries and arterioles and the smooth muscle membrane potential changes expected at different levels of sympathetic nerve activity

1983 ◽  
Vol 220 (1219) ◽  
pp. 237-249 ◽  
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Membrane ◽  
Nerve Activity ◽  
Release Of Noradrenaline ◽  
Small Arteries ◽  
Perivascular Nerves ◽  
Smooth Muscle Membrane

The membrane potential changes in arterial smooth muscle due to natural sympathetic nerve activity have been calculated. The electrical properties of the smooth muscle syncytium were taken into account and various assumptions made concerning the release of noradrenaline by the perivascular nerves. The depolarization that would result from asynchronous nerve activity at various mean frequencies was calculated for arterioles and small arteries of various diameters up to 150 μm. The calculations suggested that the depolarization would be irregular and that discrete excitatory junction potentials as evoked by synchronous nerve stimulation would not be recorded during natural nerve activity. The irregularity of the depolarization would be greater in small arterioles and would cause them to reach threshold for action potential generation at lower frequencies of nerve activity than larger arteries.

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