Electromechanical effects of endothelin on ferret bronchial and tracheal smooth muscle

1990 ◽  
Vol 68 (1) ◽  
pp. 417-420 ◽  
Author(s):  
H. K. Lee ◽  
G. D. Leikauf ◽  
N. Sperelakis
Keyword(s):  
Smooth Muscle ◽  
Slow Wave ◽  
Smooth Muscles ◽  
Muscle Cells ◽  
Wave Activity ◽  
Slow Wave Activity ◽  
Resting Potential ◽  
Base Line ◽  
Dependent Manner ◽  
Bronchial Cells

The effects of endothelin (ET) on transmembrane potential and isometric force were studied in ferret bronchial and tracheal smooth muscles. At rest, the muscle cells were electrically and mechanically quiescent. The mean resting potential for the bronchial cells was -70 +/- 1 mV (n = 25 cells/8 ferrets), and that of the tracheal cells was -60 +/- 1 mV (n = 7 cells/2 ferrets). ET depolarized and contracted both types of muscle cells in a concentration-dependent manner. At 1 nM ET, the bronchial muscle cells were significantly depolarized with concomitant force generation. In contrast, greater than 30 nM ET was required for the tracheal muscle cells to respond. The bronchial cells were further depolarized by 10 and 100 nM ET with electrical slow-wave activity present. The calcium channel antagonist verapamil substantially inhibited the contractions produced by 100 nM ET and abolished the slow-wave activity without affecting the base-line depolarization. Pretreatment of the bronchial muscle with 30 microM indomethacin did not affect the ET-induced contraction. These results suggest that ET modulates airway smooth muscle tone by direct activation and/or depolarization-induced activation of sarcolemmal calcium channels.

Effects of methylene blue on rhythmic activity and membrane potential in the canine proximal colon

1989 ◽  
Vol 256 (4) ◽  
pp. G779-G784 ◽  
Author(s):  
K. M. Sanders ◽  
E. P. Burke ◽  
R. J. Stevens
Keyword(s):  
Methylene Blue ◽  
Slow Wave ◽  
Specific Effect ◽  
Muscle Cells ◽  
Proximal Colon ◽  
Wave Activity ◽  
Slow Wave Activity ◽  
Resting Potential ◽  
Colon Cells ◽  
Circular Layer

The hypothesis that methylene blue has a direct effect on colonic muscle cells was tested. Intracellular recordings were made from cross-sectional preparations of canine proximal colon. Cells through the circular layer were impaled and membrane potentials ranging from -81 mV at the submucosal surface to -46 mV at the myenteric border were recorded. Methylene blue (10(-5) M) depolarized cells near the submucosal border by an average of 43 mV and slow-wave activity ceased. The loss of slow-wave activity could be explained by the depolarizing effects of methylene blue rather than a specific effect of methylene blue on the pacemaker mechanism. Other experiments suggested that the depolarizing effects of methylene blue were not confined to muscle cells within the submucosal pacemaker region. Depolarization of cells was noted throughout the circular layer, but the magnitude of the depolarization decreased with distance from the submucosal border. After methylene blue, the gradient in resting potential across the circular layer was greatly reduced or abolished. The data suggest that methylene blue is not necessarily a specific probe for interstitial cells and has direct effects on smooth muscle cells in the canine proximal colon. This effect is similar to treatments that are known to block the electrogenic sodium pump.

Beta-adrenergic actions on membrane electrical properties of dissociated smooth muscle cells

1988 ◽  
Vol 254 (3) ◽  
pp. C423-C431 ◽  
Author(s):  
H. Yamaguchi ◽  
T. W. Honeyman ◽  
F. S. Fay
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Electrical Properties ◽  
Smooth Muscle Cells ◽  
Input Resistance ◽  
Muscle Cells ◽  
Resting Potential ◽  
Equilibrium Potential ◽  
Dependent Manner ◽  
Beta Adrenergic

Studies were carried out to determine the effects of the beta-adrenergic agent, isoproterenol (ISO), on membrane electrical properties in single smooth muscle cells enzymatically dispersed from toad stomach. In cells bathed in buffer of physiological composition, the average resting potential was -56.4 +/- 1.4 mV (mean +/- SE, n = 35). The dominant effect of exposure to ISO was hyperpolarization. The hyperpolarization was apparent in all cells studied and averaged 11.6 +/- 1.2 mV (n = 27). In the majority of the cells, hyperpolarization was accompanied by a decreased input resistance (Rin). Often the change in resistance appeared to lag behind the change in membrane potential. The lack of coincident changes in membrane potential and resistance may reflect a superposition of the outward rectification properties of the membrane on beta-adrenergic-induced increases in ionic conductance. In about half of the cells, an initial small depolarization (3.1 +/- 0.3 mV, n = 14) was accompanied by a small but distinct increase in Rin (12 +/- 2.5%). When membrane potential was made more negative than the estimated equilibrium potential for K+ (EK) by injection of current, ISO also produced biphasic effects, an initial hyperpolarization which reversed to a sustained depolarization to a value (-90 mV) near the estimated EK. The hyperpolarization by ISO could be diminished in a time-dependent manner by previous exposure to ouabain. The inhibition by ouabain, however, appeared to be a fortuitous result of glycoside-induced positive shifts in EK. These observations indicate that the dominant electrophysiological effect of beta-adrenergic stimuli is to hyperpolarize the cell membrane.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of cromakalim and lemakalim on slow waves and membrane currents in colonic smooth muscle

1991 ◽  
Vol 260 (2) ◽  
pp. C375-C382 ◽  
Author(s):  
J. M. Post ◽  
R. J. Stevens ◽  
K. M. Sanders ◽  
J. R. Hume
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Slow Wave ◽  
Outward Current ◽  
Wave Activity ◽  
Slow Waves ◽  
Slow Wave Activity ◽  
Ca Current ◽  
K Current ◽  
Stimulation Of

The effects of cromakalim (BRL 34915) and its optical isomer lemakalim (BRL 38227) were investigated in intact tissue and freshly dispersed circular muscle cells from canine proximal colon. Cromakalim and lemakalim hyperpolarized resting membrane potential, shortened the duration of slow waves by abolishing the plateau phase, and decreased the frequency of slow waves. Glyburide, a K channel blocker, prevented the effect of cromakalim on slow-wave activity. The mechanisms of these alterations in slow-wave activity were studied in isolated myocytes under voltage-clamp conditions. Cromakalim and lemakalim increased the magnitude of a time-independent outward K current, but cromakalim also reduced the peak outward K current. Glyburide inhibited lemakalim stimulation of the time-independent background current. Nisoldipine also reduced the peak outward current, and in the presence of nisoldipine, cromakalim did not affect the peak outward component of current. This suggested that cromakalim may block a Ca-dependent component of the outward current. Lemakalim did not affect the peak outward current. We tested whether the effects of cromakalim on outward current might be indirect due to an effect on inward Ca current. Cromakalim, but not lemakalim, was found to inhibit L-type Ca channels; however, glyburide did not alter cromakalim inhibition of inward Ca current. We conclude that the effects of cromakalim and lemakalim on membrane potential and slow waves in colonic smooth muscle appear to result primarily from stimulation of a time-independent background K conductance. The effects of these compounds on channel activity may explain the inhibitory effect of these compounds on contractile activity.

Growth hormone-releasing hormone antibodies suppress sleep and prevent enhancement of sleep after sleep deprivation

1992 ◽  
Vol 263 (5) ◽  
pp. R1078-R1085 ◽  
Author(s):  
F. Obal ◽  
L. Payne ◽  
M. Opp ◽  
P. Alfoldi ◽  
L. Kapas ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Sleep Deprivation ◽  
Slow Wave ◽  
Brain Temperature ◽  
Wave Activity ◽  
Slow Wave Activity ◽  
Base Line ◽  
Light Cycle ◽  
Growth Hormone Releasing Hormone ◽  
Releasing Hormone

Previous reports suggest that the hypothalamic growth hormone-releasing hormone (GHRH) promotes sleep, especially non-rapid-eye-movement sleep (NREMS). To evaluate the role of endogenous GHRH in sleep regulation, the effects of antibodies to rat GHRH (GHRH-ab) were studied on normal sleep, brain temperature (Tbr), and GH secretion in experiment I and on enhanced sleep after sleep deprivation in experiment II. In experiment I, affinity-purified GHRH-ab (50 and 200 micrograms) raised in goats and a control goat immunoglobulin G (IgG) preparation were injected intracerebroventricularly (icv) in rats 1 h before the onset of the light cycle, and sleep-wake activity and Tbr were recorded for the next 12 or 23 h. Both doses of GHRH-ab suppressed NREMS and REMS throughout the light cycle. Sleep durations at night were normal. Electroencephalographic (EEG) slow-wave activity, characterized by EEG slow-wave amplitudes, was reduced after GHRH-ab during both the light and the dark cycles. Plasma GH concentrations measured 6-12 h after injection of GHRH-ab (200 micrograms) were diminished. Both the control IgG and GHRH-ab elicited fever. In experiment II, the sleep-wake activity and Tbr of rats were recorded for 24 h in three experimental conditions: base-line with icv injection of IgG, 3-h sleep deprivation with icv IgG injection, and 3-h sleep deprivation with icv GHRH-ab (200 micrograms). After sleep deprivation (+IgG), a prompt increase in EEG slow-wave activity (power density analysis) and late increases in NREMS and REMS durations were found.(ABSTRACT TRUNCATED AT 250 WORDS)

Selective lesioning of interstitial cells of Cajal by methylene blue and light leads to loss of slow waves

1994 ◽  
Vol 266 (3) ◽  
pp. G485-G496 ◽  
Author(s):  
L. W. Liu ◽  
L. Thuneberg ◽  
J. D. Huizinga
Keyword(s):  
Methylene Blue ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Electrical Activity ◽  
Slow Wave ◽  
Interstitial Cells Of Cajal ◽  
Wave Activity ◽  
Slow Waves ◽  
Slow Wave Activity ◽  
Cells Of Cajal

Incubation with 50 microM methylene blue (MB) and subsequent intense illumination resulted in abolition of the slow-wave activity in the submuscular interstitial cells of Cajal-circular muscle (ICC-CM) preparations of canine colon. This was often accompanied by a decrease in resting membrane potential. Repolarization of cells back to -70 mV did not restore the slow-wave activity, indicating that MB plus light directly interrupted the generation mechanism of slow waves. After MB incubation, a 2-min illumination consistently changed the mitochondrial conformation in ICCs from very condensed to orthodox, without inducing any obvious changes in smooth muscle cells. After 4- to 10-min illumination, ICCs became progressively more damaged with swollen and ruptured mitochondria, loss of cytoplasmic contrast and detail, loss of caveolae, and rupture of the plasma membrane. No damage was seen in smooth muscle cells or nerves. Gap junctional ultrastructure was preserved. Intense illumination without preincubation with MB left the slow waves and the ultrastructure of ICC-CM preparations unaffected. In CM preparations, without the submuscular ICC-smooth-muscle network, MB plus light induced no changes in electrical activity. We conclude that the correlation between selective damage to the submuscular ICCs (relative to smooth muscle) and selective loss of the slow-wave activity (relative to other electrical activity of the CM) strongly indicates that the ICCs play an essential role in the generation of slow waves.

scholarly journals Effects of Ursolic Acid on Contractile Activity of Gastric Smooth Muscles

2015 ◽  
Vol 10 (4) ◽  
pp. 1934578X1501000 ◽  
Author(s):  
Natalia Prissadova ◽  
Petko Bozov ◽  
Kiril Marinkov ◽  
Hristo Badakov ◽  
Atanas Kristev
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Ursolic Acid ◽  
Slow Wave ◽  
Contractile Activity ◽  
Smooth Muscles ◽  
Dependent Manner ◽  
Krebs Solution ◽  
Concentration Dependent Manner ◽  
Gastric Smooth Muscle

Ursolic acid (UA) in concentrations of 1×10−7 mol/L - 5×10−5 mol/L induced relaxation in gastric smooth muscle (SM) tissues, in a concentration-dependent manner. The relaxation did not change membrane potential and slow wave contraction patterns. A significant decrease in amplitude and frequency of spike-potentials was observed. UA-induced reactivity was removed when SM preparations were treated with nifedipine (1×10−6 mol/L). Ca2+- induced contractions of the depolarized SM preparations (42 mmol/L K+; Ca2+- free Krebs solution) were substantially reduced in the presence of UA. It was determined that, in certain concentrations, UA influenced L – type Ca2+ channels, and reduced the Ca2+ influx.

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)

scholarly journals Human smooth muscle VLA-1 integrin: purification, substrate specificity, localization in aorta, and expression during development.

1990 ◽  
Vol 111 (5) ◽  
pp. 2159-2170 ◽  
Author(s):  
V M Belkin ◽  
A M Belkin ◽  
V E Koteliansky
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Smooth Muscles ◽  
Muscle Cells ◽  
Type I ◽  
Dependent Manner ◽  
Aortic Smooth Muscle Cells ◽  
Aortic Smooth Muscle ◽  
Sds Page ◽  
Aortic Media

A membrane glycoprotein complex was isolated and purified from human smooth muscle by detergent solubilization and affinity chromatography on collagen-Sepharose. The complex was identified as VLA-1 integrin and consisted of two subunits of 195 and 130 kD in SDS-PAGE. Liposomes containing the VLA-1 integrin adhered to surfaces coated with type I, II, III, and IV collagens, Clq subcomponent of the first component of the complement, and laminin. The liposomes specifically adhered to these proteins in a Ca2+, Mg2(+)-dependent manner, but did not bind to gelatin, fibronectin, and thrombospondin substrates. The expression of VLA-1 integrin in different human tissues and cell types, and during aorta smooth muscle development was studied by SDS-PAGE, and subsequent quantitative immunoblotting was performed with antibodies recognizing alpha 1 and beta 1 subunits of the VLA-1 integrin. A high level of VLA-1 integrin expression was an exceptional feature of smooth muscles. Fibroblasts, endothelial cells, keratinocytes, striated muscles, and platelets contained trace amounts of VLA-1 integrin. In the 10-wk-old human fetal aorta, VLA-1 integrin was found only in smooth muscle cells whereas mesenchymal cells, surrounding aortic smooth muscle cells, were VLA-1 integrin negative. By the 24th wk of gestation, the amount of VLA-1 integrin was significantly reduced in the aortic media (4.3-fold for alpha 1 subunit and 2.5-fold for beta 1 subunit) compared with that in the 10-wk-old aortic smooth muscle cells. After birth, the expression of VLA-1 integrin increased and in the 1.5-yr-old child aorta the VLA-1 integrin level was almost the same as in adult aortic media. Smooth muscle cells from intimal thickening of adult aorta express five times less alpha 1 subunit of VLA integrin that smooth muscle cells from adult aortic media. In primary culture of aortic smooth muscle cells, the content of the VLA-1 integrin was dramatically reduced and subcultured cells did not contain VLA-1 integrin at all.

scholarly journals Input zone-selective dysrhythmia in motor thalamus after dopamine depletion

2021 ◽  
Author(s):  
Kouichi C. Nakamura ◽  
Andrew Sharott ◽  
Takuma Tanaka ◽  
Peter J. Magill
Keyword(s):  
Basal Ganglia ◽  
Slow Wave ◽  
Wave Activity ◽  
Slow Wave Activity ◽  
Brain State ◽  
Dependent Manner ◽  
Dopamine Depletion ◽  
Beta Band ◽  
Beta Oscillations ◽  
Motor Thalamus

AbstractThe cerebral cortex, basal ganglia and motor thalamus form circuits important for purposeful movement. In Parkinsonism, basal ganglia neurons often exhibit dysrhythmic activity during, and with respect to, the slow (∼1 Hz) and beta-band (15–30 Hz) oscillations that emerge in cortex in a brain state-dependent manner. There remains, however, a pressing need to elucidate the extent to which motor thalamus activity becomes similarly dysrhythmic after dopamine depletion relevant to Parkinsonism. To address this, we recorded single-neuron and ensemble outputs in the ‘basal ganglia-recipient zone’ (BZ) and ‘cerebellar-recipient zone’ (CZ) of motor thalamus in anesthetized male dopamine-intact rats and 6-OHDA-lesioned rats during two brain states, respectively defined by cortical slow-wave activity and activation. Two forms of thalamic input zone-selective dysrhythmia manifested after dopamine depletion: First, BZ neurons, but not CZ neurons, exhibited abnormal phase-shifted firing with respect to cortical slow oscillations prevalent during slow-wave activity; secondly, BZ neurons, but not CZ neurons, inappropriately synchronized their firing and engaged with the exaggerated cortical beta oscillations arising in activated states. These dysrhythmias were not accompanied by the thalamic hypoactivity predicted by canonical firing rate-based models of circuit organization in Parkinsonism. Complementary recordings of neurons in substantia nigra pars reticulata suggested their altered activity dynamics could underpin the BZ dysrhythmias. Finally, pharmacological perturbations demonstrated that ongoing activity in the motor thalamus bolsters exaggerated beta oscillations in motor cortex. We conclude that BZ neurons are selectively primed to mediate the detrimental influences of abnormal slow and beta-band rhythms on circuit information processing in Parkinsonism.

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