Voltage-gated Ca2+ currents are necessary for slow-wave propagation in the canine gastric antrum

2007 ◽  
Vol 293 (5) ◽  
pp. C1645-C1659 ◽  
Author(s):  
Orline Bayguinov ◽  
Sean M. Ward ◽  
James L. Kenyon ◽  
Kenton M. Sanders
Keyword(s):  
Wave Propagation ◽  
Slow Wave ◽  
Propagation Velocity ◽  
Circular Muscle ◽  
Slow Waves ◽  
Dependent Manner ◽  
Voltage Dependent ◽  
Lesser Curvature ◽  
Propagation Velocities ◽  
Upstroke Velocity

Electrical slow waves determine the timing and force of peristaltic contractions in the stomach. Slow waves originate from a dominant pacemaker in the orad corpus and propagate actively around and down the stomach to the pylorus. The mechanism of slow-wave propagation is controversial. We tested whether Ca2+ entry via a voltage-dependent, dihydropyridine-resistant Ca2+ conductance is necessary for active propagation in canine gastric antral muscles. Muscle strips cut parallel to the circular muscle were studied with intracellular electrophysiological techniques using a partitioned-chamber apparatus. Slow-wave upstroke velocity and plateau amplitude decreased from the greater to the lesser curvature, and this corresponded to a decrease in the density of interstitial cells of Cajal in the lesser curvature. Slow-wave propagation velocity between electrodes impaling cells in two regions of muscle and slow-wave upstroke and plateau were measured in response to experimental conditions that reduce the driving force for Ca2+ entry or block voltage-dependent Ca2+ currents. Nicardipine (0.1–1 μM) did not affect slow-wave upstroke or propagation velocities. Upstroke velocity, amplitude, and propagation velocity were reduced in a concentration-dependent manner by Ni2+ (1–100 μM), mibefradil (10–30 μM), and reduced extracellular Ca2+ (0.5–1.5 mM). Depolarization (by 10–15 mM K+) or hyperpolarization (10 μM pinacidil) also reduced upstroke and propagation velocities. The higher concentrations (or lowest Ca2+) of these drugs and ionic conditions tested blocked slow-wave propagation. Treatment with cyclopiazonic acid to empty Ca2+ stores did not affect propagation. These experiments show that voltage-dependent Ca2+ entry is obligatory for the upstroke phase of slow waves and active propagation.

Voltage sensitivity of slow wave frequency in isolated circular muscle strips from guinea pig gastric antrum

1999 ◽  
Vol 276 (2) ◽  
pp. G518-G528 ◽  
Author(s):  
S.-M. Huang ◽  
S. Nakayama ◽  
S. Iino ◽  
T. Tomita
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Slow Wave ◽  
Circular Muscle ◽  
Gastric Antrum ◽  
Slow Waves ◽  
Wave Frequency ◽  
Voltage Sensitivity ◽  
Dependent Manner ◽  
Circular Smooth Muscle

In circular muscle preparations isolated from the guinea pig gastric antrum, regular spontaneous electrical activity (slow waves) was recorded. Under normal conditions (6 mM K+), the frequency and shape of the slow waves were similar to those observed in ordinary stomach smooth muscle preparations. When the resting membrane potential was hyperpolarized and depolarized by changing the extracellular K+ concentration (2–18 mM), the frequency of slow waves decreased and increased, respectively. Application of cromakalim hyperpolarized the cell membrane and reduced the frequency of slow waves in a dose-dependent manner. Cromakalim (3 μM) hyperpolarized the membrane, and slow waves ceased in most preparations. In the presence of cromakalim, subsequent increases in the extracellular K+ concentration restored the frequency of slow waves accompanied by depolarization. Also, glibenclamide completely antagonized this effect of cromakalim. In smooth muscle strips containing both circular and longitudinal muscle layers, such changes in the slow wave frequency were not observed. It was concluded that the maneuver of isolating circular smooth muscle altered the voltage dependence of the slow wave frequency.

Electrical slow-wave activity from the circular layer of cat terminal antrum

1991 ◽  
Vol 261 (1) ◽  
pp. G78-G82
Author(s):  
L. M. Renzetti ◽  
M. B. Wang ◽  
J. P. Ryan
Keyword(s):  
Slow Wave ◽  
Circular Muscle ◽  
Muscle Cells ◽  
Muscle Layer ◽  
Wave Activity ◽  
Slow Waves ◽  
Slow Wave Activity ◽  
Plateau Phase ◽  
Circular Layer ◽  
Upstroke Velocity

Intracellular recording techniques were used to characterize the electrical slow-wave activity through the thickness of the circular muscle layer of the cat terminal antrum. Muscle strips were pinned out in cross section to the floor of a recording chamber perfused with Krebs buffer. Circular muscle cells from the myenteric to the submucosal border then were impaled with 20- to 40-M omega glass microelectrodes, and slow-wave activity was recorded. Slow waves from the myenteric side of the circular layer consisted of an upstroke depolarization, a prominent plateau phase, and a downstroke repolarization. Slow-wave characteristics for cells along the myenteric border were Em, -74.2 +/- 1.3 mV; duration, 5.3 +/- 0.5 s; upstroke amplitude, 29.4 +/- 3.4 mV; upstroke velocity, 0.20 +/- 0.03 V/s; and frequency, 5.8 +/- 0.5/min. Slow waves from muscle cells along the submucosal side of the preparation lacked a discernible plateau phase. Slow waves from submucosal border cells had the following characteristics: Em, -80.4 +/- 1.4 mV (P less than 0.01); duration, 3.5 +/- 0.4 s (P less than 0.01); upstroke amplitude, 44.0 +/- 2.4 mV (P less than 0.01); upstroke velocity, 0.56 +/- 0.06 V/s (P less than 0.01); and frequency, 4.2 +/- 0.4/min (P less than 0.05). Slow waves were not affected by 10(-7)M tetrodotoxin and 10(-6)M atropine or by removal of the longitudinal muscle layer. Slow-wave activity within each region was maintained after dissecting the circular layer into submucosal and myenteric segments. The results suggest that two distinct slow waves exist within the circular muscle layer of the cat terminal antrum.(ABSTRACT TRUNCATED AT 250 WORDS)

Origin and spread of slow waves in canine gastric antral circular muscle

1985 ◽  
Vol 249 (6) ◽  
pp. G800-G806 ◽  
Author(s):  
A. J. Bauer ◽  
N. G. Publicover ◽  
K. M. Sanders
Keyword(s):  
Wave Propagation ◽  
Slow Wave ◽  
Myenteric Plexus ◽  
Circular Muscle ◽  
Slow Waves ◽  
Three Dimensions ◽  
Muscle Strip ◽  
Velocity Measurements ◽  
Conduction Velocities ◽  
Axis Parallel

Electrical slow waves recorded from circular muscle cells near the myenteric and submucosal plexuses were found to be significantly different. By measuring the latencies between the arrival of evoked events at two recording sites, slow wave conduction velocities were determined in the three dimensions of circular muscle. Slow waves propagated more rapidly in the axis parallel to the circular fibers than in the axes perpendicular to the circular fibers. The rates of slow wave propagation were also determined in axes parallel and perpendicular to fibers in myenteric and submucosal circular muscles. Slow waves conducted more slowly in the circular muscle near the submucosa than in circular muscle near the myenteric plexus. From conduction velocity measurements, a technique was developed to determine the pacemaker site of spontaneous slow waves in a muscle strip. These data demonstrate that slow waves originate from multiple discrete foci; in muscle strips cut along the long axis of the stomach, these foci are found predominantly in the orad region of the muscle strip; and slow waves originate in the outer myenteric half of the muscle.

scholarly journals Abnormal gastric slow waves in patients with functional dyspepsia assessed by multichannel electrogastrography

2001 ◽  
Vol 280 (6) ◽  
pp. G1370-G1375 ◽  
Author(s):  
Xuemei Lin ◽  
Jiande Z. Chen
Keyword(s):  
Wave Propagation ◽  
Functional Dyspepsia ◽  
Slow Wave ◽  
Single Channel ◽  
Slow Waves ◽  
Lower Percentage ◽  
Healthy Controls ◽  
Fasting State ◽  
Gastric Slow Wave ◽  
Gastric Slow Waves

The aim of this study was to utilize multichannel electrogastrography to investigate whether patients with functional dyspepsia had impaired propagation or coordination of gastric slow waves in the fasting state compared with healthy controls. The study was performed in 10 patients with functional dyspepsia and 11 healthy subjects. Gastric myoelectrical activity was measured by using surface electrogastrography with a specially designed four-channel device. The study was performed for 30 min or more in the fasting state. Special computer programs were developed for the computation of the propagation and coupling of the gastric slow wave. It was found that, compared with the healthy controls, the patients showed a significantly lower percentage of slow wave propagation (58.0 ± 8.9 vs. 89.9 ± 2.6%, P < 0.002) and a significantly lower percentage of slow wave coupling (46.9 ± 4.4 vs. 61.5 ± 6.9%, P < 0.04). In addition, the patients showed inconsistencies in the frequency and regularity of the gastric slow wave among the four-channel electrogastrograms (EGGs). It was concluded that patients with functional dyspepsia have impaired slow wave propagation and coupling. Multichannel EGG has more information than single-channel EGG for the detection of gastric myoelectrical abnormalities.

Pacemaker activity in septal structures of canine colonic circular muscle

1990 ◽  
Vol 259 (2) ◽  
pp. G264-G273 ◽  
Author(s):  
S. M. Ward ◽  
K. M. Sanders
Keyword(s):  
Slow Wave ◽  
Electrical Coupling ◽  
Circular Muscle ◽  
Proximal Colon ◽  
Slow Waves ◽  
Pacemaker Activity ◽  
Electrical Measurements ◽  
Morphological Studies ◽  
Circular Layer ◽  
And Function

Morphological and electrophysiological experiments were performed to characterize the pacemaker areas of the circular muscle in the canine proximal colon. Morphological studies showed interstitial cells of Cajal lining the submucosal surface of the circular layer and the septal structures that separate the circular layer into bundles. Electrical measurements suggested that slow waves may propagate into the thickness of the circular muscle in a regenerative manner along the surface of these septa. Removal of the submucosal pacemaker region blocked generation of slow waves in nonseptal regions of the circular muscle, but slow-wave activity continued in the circular muscle near septa. These data suggest that slow-wave pacemaker activity is not limited to a two-dimensional surface at the submucosal surface but extends into the interior of the circular layer along septal invaginations. Experiments were also performed to determine the dominance of pacemaker activity (i.e., septal vs. submucosal), and examples were found in which both areas appeared to initiate slow waves in intact muscles. Other studies showed that slow waves could propagate across septa, suggesting some form of electrical coupling between circular muscle bundles. This study provides a more complete view of the structure and function of pacemaker areas in the canine proximal colon.

Myogenic mechanism for peristalsis in the cat esophagus

1999 ◽  
Vol 277 (2) ◽  
pp. G306-G313 ◽  
Author(s):  
Harold G. Preiksaitis ◽  
Nicholas E. Diamant
Keyword(s):  
Muscle Contraction ◽  
Slow Wave ◽  
Circular Muscle ◽  
Smooth Muscle Contraction ◽  
Slow Waves ◽  
Mechanical Activity ◽  
Control Mechanisms ◽  
Slow Wave Oscillations

A myogenic control system (MCS) is a fundamental determinant of peristalsis in the stomach, small bowel, and colon. In the esophagus, attention has focused on neuronal control, the potential for a MCS receiving less attention. The myogenic properties of the cat esophagus were studied in vitro with and without nerves blocked by 1 μM TTX. Muscle contraction was recorded, while electrical activity was monitored by suction electrodes. Spontaneous, nonperistaltic, electrical, and mechanical activity was seen in the longitudinal muscle and persisted after TTX. Spontaneous circular muscle activity was minimal, and peristalsis was not observed without pharmacological activation. Direct electrical stimulation (ES) in the presence of bethanechol or tetraethylammonium chloride (TEA) produced slow-wave oscillations and spike potentials accompanying smooth muscle contraction that progressed along the esophagus. Increased concentrations of either drug in the presence of TTX produced slow waves and spike discharges, accompanied by peristalsis in 5 of 8 TEA- and 2 of 11 bethanechol-stimulated preparations without ES. Depolarization of the muscle by increasing K+ concentration also produced slow waves but no peristalsis. We conclude that the MCS in the esophagus requires specific activation and is manifest by slow-wave oscillations of the membrane potential, which appear to be necessary, but are not sufficient for myogenic peristalsis. In vivo, additional control mechanisms are likely supplied by nerves.

Slow waves actively propagate at submucosal surface of circular layer in canine colon

1990 ◽  
Vol 259 (2) ◽  
pp. G258-G263 ◽  
Author(s):  
K. M. Sanders ◽  
R. Stevens ◽  
E. Burke ◽  
S. W. Ward
Keyword(s):  
Wave Propagation ◽  
Slow Wave ◽  
Proximal Colon ◽  
Slow Waves ◽  
Pacemaker Cells ◽  
Transverse Axis ◽  
Active Mechanism ◽  
Conduction Velocities ◽  
Circular Layer ◽  
Thin Band

Colonic slow waves originate from pacemaker cells along the submucosal surface of the circular layer in the dog proximal colon. These events propagate in a nonregenerative manner into the bulk of the circular layer. Conduction velocities consistent with an active mechanism for slow-wave propagation in the longitudinal and circumferential axes of the colon have been reported. Experiments were performed using intracellular recording techniques on canine colonic muscles to determine the regenerative pathway for slow-wave propagation. In a thin band of muscle adjacent to the submucosal border of the circular layer, slow-wave amplitude was independent of distance from a pacing source, and events propagated at a rate of approximately 17 mm/s in the long axis of the circular fibers and 6 mm/s in the transverse axis of the circular fibers. These findings suggest that slow waves propagate in a regenerative manner in this region. Slow waves decayed as they conducted through regions from which the pacemaker cells had been removed with space constants of a few millimeters. Thus the integrity of the thin pacemaker region along submucosal surface is critical for propagation of slow waves and the organization of motility into segmental contractions.

Myogenic regulation of propagation in gastric smooth muscle

1985 ◽  
Vol 248 (5) ◽  
pp. G512-G520 ◽  
Author(s):  
N. G. Publicover ◽  
K. M. Sanders
Keyword(s):  
Wave Propagation ◽  
Conduction Velocity ◽  
Circular Muscle ◽  
Slow Waves ◽  
Gastric Distension ◽  
Gastric Smooth Muscle ◽  
Conduction Velocities ◽  
Axis Parallel ◽  
Myogenic Regulation

Experiments were performed to test the effects of frequency and stretch on the velocity of slow wave propagation parallel and perpendicular to the long axis of circular muscle fibers in the canine gastric antrum. Slow waves were evoked from one corner of a rectangular sheet of muscle and propagated throughout the tissue. Mathematics were derived and are presented, which simultaneously compute conduction velocities in each direction, regardless of electrode positions. Increased rate of stimulation had no significant effect on conduction velocity in the circumferential axis, but propagation slowed in the axis perpendicular to the circular fibers by an average of 25% over interstimulus intervals between 12 and 60 s. Conduction velocity was also a function of the degree of stretch. The most rapid conduction velocity occurred when muscles were stretched to an average of 118% of the resting, fasted length found in situ in the axis parallel to the circular fibers and 140% in the axis perpendicular to the circular fibers. Propagation was blocked by stretching muscles past 200% of resting length. These results suggest that the frequency of slow waves and gastric distension are intrinsic mechanisms capable of regulating the spread of slow waves.

Postprandial changes in intestinal slow-wave propagation reflect a decrease in cell coupling

1989 ◽  
Vol 257 (3) ◽  
pp. G463-G469
Author(s):  
D. Terasaka ◽  
A. Bortoff ◽  
L. F. Sillin
Keyword(s):  
Wave Propagation ◽  
Electrical Activity ◽  
Slow Wave ◽  
Propagation Velocity ◽  
Maximum Rate ◽  
Internal Resistance ◽  
Cell Coupling ◽  
Wave Propagation Velocity ◽  
Fasting Level ◽  
Amplitude Maximum

The purpose of these studies was to determine the effects of feeding on jejunal slow-wave propagation velocity (SWPV). Nine cats were instrumented with six pairs of electrodes implanted 4 cm apart on the jejunum. Electrical activity was recorded at the end of an 18-h fast after which each animal was fed 60 g of canned cat food. Recordings were continued during feeding and for several hours thereafter. This procedure was repeated at least twice for each cat. Average SWPV (cm/s) decreased from a fasting level of 2.28 +/- 0.20 (mean of means +/- SE) to 1.93 +/- 0.16 at 10-20 min, 1.51 +/- 0.11 at 1 h, and 1.37 +/- 0.10 at 3 h postprandially. Corresponding SW frequencies (SWFs) were 19.6 +/- 0.3, 18.7 +/- 0.2, 19.2 +/- 0.2, and 19.0 +/- 0.2 cycles/min, respectively. The differences between the fasting SWPV and that at 1 and 3 h were significant (P less than 0.05). When SWPV was plotted as a function of SWF, the slopes of the corresponding curves were also found to decrease postprandially (P less than 0.05, fasting vs. 1 and 3 h). There was no apparent change in SW amplitude, maximum rate of SW depolarization, or threshold. In the absence of changes in these parameters, the divergence of the slopes at lower SWFs indicates that the decrease in SWPV is because of increased internal resistance, probably the result of uncoupling of intestinal muscle cells. The change is rapid in onset and long in duration, suggesting that an uncoupling factor is released during ingestion of a meal, and that its effect persists for several hours.

Pacemaker potentials generated by interstitial cells of Cajal in the murine intestine

2005 ◽  
Vol 288 (3) ◽  
pp. C710-C720 ◽  
Author(s):  
Yoshihiko Kito ◽  
Sean M. Ward ◽  
Kenton M. Sanders
Keyword(s):  
Interstitial Cells Of Cajal ◽  
Circular Muscle ◽  
Muscle Cells ◽  
Interstitial Cells ◽  
Slow Waves ◽  
Pacemaker Activity ◽  
Dependent Manner ◽  
Plateau Potential ◽  
Pacemaker Potentials ◽  
Cells Of Cajal

Pacemaker potentials were recorded in situ from myenteric interstitial cells of Cajal (ICC-MY) in the murine small intestine. The nature of the two components of pacemaker potentials (upstroke and plateau) were investigated and compared with slow waves recorded from circular muscle cells. Pacemaker potentials and slow waves were not blocked by nifedipine (3 μM). In the presence of nifedipine, mibefradil, a voltage-dependent Ca2+ channel blocker, reduced the amplitude, frequency, and rate of rise of upstroke depolarization (d V/d tmax) of pacemaker potentials and slow waves in a dose-dependent manner (1–30 μM). Mibefradil (30 μM) changed the pattern of pacemaker potentials from rapidly rising, high-frequency events to slowly depolarizing, low-frequency events with considerable membrane noise (unitary potentials) between pacemaker potentials. Caffeine (3 mM) abolished pacemaker potentials in the presence of mibefradil. Pinacidil (10 μM), an ATP-sensitive K+ channel opener, hyperpolarized ICC-MY and increased the amplitude and d V/d tmax without affecting frequency. Pinacidil hyperpolarized smooth muscle cells and attenuated the amplitude and d V/d tmax of slow waves without affecting frequency. The effects of pinacidil were blocked by glibenclamide (10 μM). These data suggest that slow waves are electrotonic potentials driven by pacemaker potentials. The upstroke component of pacemaker potentials is due to activation of dihydropyridine-resistant Ca2+ channels, and this depolarization entrains pacemaker activity to create the plateau potential. The plateau potential may be due to summation of unitary potentials generated by individual or small groups of pacemaker units in ICC-MY. Entrainment of unitary potentials appears to depend on Ca2+ entry during upstroke depolarization.

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