The effect of diazepam on potassium contractures, contraction threshold, and resting tension in rat skeletal muscles

1988 ◽  
Vol 66 (5) ◽  
pp. 573-579 ◽  
Author(s):  
Michael Chua ◽  
Angela F. Dulhunty
Keyword(s):  
Membrane Potential ◽  
Type Equation ◽  
Resting Membrane Potential ◽  
Muscle Fibres ◽  
High Potassium ◽  
Fourfold Increase ◽  
Maximum Tension ◽  
Potassium Contracture ◽  
Negative Shift ◽  
Resting Tension

The effects of diazepam on potassium contractures, contraction threshold, and resting tension have been examined in rat soleus muscle fibres. Two actions of the drug were defined that could not be attributed to changes in the resting membrane potential or depolarization in high potassium solutions. The major effect was an increase in the amplitude of submaximal tension during either twitches or potassium contractures and an increase in resting tension. At 400 μM diazepam, there was (a) a fourfold increase in 40 mM potassium contracture tension, (b) a negative shift of 8 mV in the membrane potential for half maximum tension estimated from the best fit of a Boltzmann-type equation to average potassium contracture data, (c) a negative shift of 8 mV in the threshold for contraction measured under voltage clamp conditions, and (d) a contracture of variable amplitude to a level that was occasionally equivalent to maximum tetanic tension. These potentiating actions of diazepam depended on drag concentration within the range of 100–800 μM. In contrast, the second effect of diazepam, depression of maximum tension by 10–15%, was independent of drug concentration between 100 and 400 μM. The results support the idea that diazepam produces an increase in resting myoplasmic calcium concentrations.

The resting membrane potential of white muscle from brown trout (Salmo trutta) exposed to copper in soft, acidic water

2000 ◽  
Vol 203 (14) ◽  
pp. 2229-2236 ◽  
Author(s):  
M.W. Beaumont ◽  
E.W. Taylor ◽  
P.J. Butler
Keyword(s):  
Membrane Potential ◽  
Brown Trout ◽  
Salmo Trutta ◽  
White Muscle ◽  
Low Ph ◽  
Ammonium Ion ◽  
Muscle Membrane ◽  
Resting Membrane Potential ◽  
Muscle Fibres ◽  
Brown Trout Salmo Trutta

Previously, the distribution of ammonia between the intracellular and extracellular compartments has been used to predict a significant depolarisation of the resting membrane potential (E(M)) of white muscle from brown trout (Salmo trutta) exposed to a sub-lethal combination of copper and low pH. However, this prediction is based upon two assumptions (i) a relatively high membrane permeability for the ammonium ion with respect to that for ammonia gas and (ii) that this is unaltered by exposure to copper and low pH. Since there is conflicting evidence in the literature of the validity of these assumptions, in the present study E(M) was directly measured in white muscle fibres of trout exposed to copper and low pH (E(M)=−52.2+/−4.9 mV) and compared with that of unexposed, control animals (E(M)=−86.5+/−2.9 mV) (means +/− s.e.m., N=6). In confirming the predicted depolarisation, these data support the hypothesis of electrophysiological impairment as a factor in the reduction in the swimming performance of trout exposed to these pollutants. In addition, the results of this study support the role of a significant permeability of the muscle membrane to NH(4)(+) in determining the distribution of ammonia in fish.

The nature of the monosynaptic excitatory and inhibitory processes in the spinal cord

1952 ◽  
Vol 140 (899) ◽  
pp. 169-176 ◽  
Keyword(s):  
Spinal Cord ◽  
Membrane Potential ◽  
Electrical Properties ◽  
Glass Tube ◽  
Giant Axon ◽  
Resting Membrane Potential ◽  
Muscle Fibres ◽  
Spike Potential ◽  
Inhibitory Processes ◽  
Fine Glass

Recently it has been possible to record electrically from motoneurones in the spinal cord of the anaesthetized cat by means of an intracellular electrode (Brock, Coombs & Eccles 1951, 1952). As with investigations on isolated nerve and muscle fibres (Ling & Gerard 1949; Nastuk & Hodgkin 1950; Weidmann 1951; Fatt & Katz 1951) the micro-electrode is a fine glass tube filled with 3 m-KCI and with a tip diameter of about 0-5 µ .Necessarily it has to be inserted ‘blindly’ into a motoneurone lying some 2 mm deep in the spinal cord. However, the position of a pool of motoneurones belonging to any one muscle is now fairly well known (Romanes 1951), and the motoneurones are made to signal their position electrically during the process of insertion by firing impulses into them antidromically and also by monosynaptically activating them. The entry of a micro-electrode into a motoneurone is immediately and unambiguously signalled by two events: the recording of the resting membrane potential (about 70 mV); the inversion and large increase in the antidromic spike potential, which gives a reversal of membrane potential of as much as 35 mV. In general, both during rest and in the propagation of impulses, the electrical properties of the motoneurone closely resemble those of the isolated giant axon.

scholarly journals Exercise training increases K+-channel contribution to regulation of coronary arterial tone

1998 ◽  
Vol 84 (4) ◽  
pp. 1225-1233 ◽  
Author(s):  
D. K. Bowles ◽  
M. H. Laughlin ◽  
M. Sturek
Keyword(s):  
Membrane Potential ◽  
Exercise Training ◽  
Sodium Nitroprusside ◽  
K Channel ◽  
Resting Membrane Potential ◽  
Channel Blockers ◽  
Miniature Swine ◽  
Isolated Cells ◽  
Resting Tension ◽  
Basal Tone

The present study examined whether regulation of coronary tone in conduit arteries (>1.0 mm ID) is altered by exercise training. Yucatan miniature swine were treadmill trained for 16–20 wk (Ex) and compared with sedentary counterparts (Sed). Endothelium-denuded arterial rings were stretched to optimal length and allowed to equilibrate for 60 min. Inhibition of either Ca2+-activated channels [1 mM tetraethylammonium (TEA) or 10 nM iberiotoxin (IBTX)] or voltage-dependent K+ channels [1 mM 4-aminopyridine (4-AP)] significantly increased resting tension in both groups; however, the effect of all K+-channel blockers was greater in Ex. Addition of 1 mM sodium nitroprusside reduced resting tension in both groups, confirming the presence of active basal tone; however, sodium nitroprusside-sensitive tone was increased approximately twofold in Ex compared with Sed group. Perforated patch-clamp experiments on isolated smooth muscle cells demonstrated no effect of exercise training on whole cell TEA-sensitive, 4-AP-sensitive, or basal K+ current. Similarly, whereas TEA, 4-AP, and IBTX all decreased resting membrane potential, there was no difference in depolarization between groups. The greater effect of TEA on resting tension in Ex could be mimicked in Sed by addition of the Ca2+-channel agonist BAY K 8644. In conclusion, the greater response to K+-channel blockers after exercise training is consistent with an increased contribution of K+ channels to regulation of basal tone in conduit coronary arteries. The lack of an effect of training on K+ current characteristics or membrane potential responses in isolated cells suggests that a requisite factor for enhanced K+-channel activation in arteries from Ex, possibly stretch, is absent in isolated cells.

Removal of the epithelium potentiates acetylcholine in depolarizing canine bronchial smooth muscle

1988 ◽  
Vol 65 (6) ◽  
pp. 2400-2405 ◽  
Author(s):  
Y. Gao ◽  
P. M. Vanhoutte
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Cell Membrane ◽  
Adrenergic Receptors ◽  
Force Transducer ◽  
Third Order ◽  
Bronchial Smooth Muscle ◽  
High Potassium ◽  
Resting Tension ◽  
Made In

Experiments were designed to determine whether the airway epithelium affects the membrane potential of the underlying smooth muscle. The effect of epithelium removal (by gentle rubbing) on the responsiveness of isolated canine bronchi was studied. Simultaneous recordings of mechanical and electrical activity were made in paired circumferential strips (with and without epithelium) of third-order bronchi. Changes in tension were recorded with a force transducer, and changes in membrane potential were measured with a microelectrode. The cell membrane potential and resting tension of the bronchial smooth muscle were stable over a 150-min period and were not affected by removal of the epithelium. In the presence of antagonists at muscarinic and adrenergic receptors, the resting tension and membrane potential were comparable in preparations with and without epithelium. By contrast, the anticholinesterase, echothiophate, caused depolarization in bronchi without epithelium. Exposure to high potassium induced similar levels of depolarization and contraction in tissues with and without epithelium. No significant differences in threshold for depolarization or for mechanical activation in the membrane potential-tension relationship were noted in the presence or absence of epithelium. In the presence of echothiophate, removal of the epithelium augmented the contraction of the bronchi to acetylcholine; the depolarization of the cell membrane induced by the cholinergic transmitter was significantly larger than in control tissues, even when matched contractions were compared. These observations indicate that the respiratory epithelium generates an inhibitory substance that dampens depolarization and contraction of bronchial smooth muscle caused by acetylcholine.

Changes in Membrane Properties of the Drosophila Dorsal Longitudinal Flight Muscle Induced by Sodium Pump Inhibitors

1981 ◽  
Vol 90 (1) ◽  
pp. 175-183 ◽  
Author(s):  
BARBARA K. HENON ◽  
KAZUO IKEDA
Keyword(s):  
Membrane Potential ◽  
Action Potentials ◽  
Sodium Pump ◽  
Flight Muscle ◽  
Input Resistance ◽  
Resting Membrane Potential ◽  
Slow Phase ◽  
Muscle Fibres ◽  
Fast Phase ◽  
In Cells

1. Drosophila dorsal longitudinal flight muscle fibres made anoxic by passing nitrogen through the tracheal system or treated with 10−5M ouabain or strophanthidin show a reversible fall in resting membrane potential of 16·5 mV (S.E. 0·96), 1·37 mV (S.E. 0·87), and 1·70 mV (S.E. 2·8), respectively. The reversible depolarization obtained with these sodium pump blockers occurred within 10–15 min. 2. The depolarization of the muscle fibres was accompanied by a decrease in input resistance of 21·2% (S.E. 3·8) in anoxia, 21·4% in ouabain, and 25·6% (S.E. 6·7) in strophanthidin. The resistance decrease in strophanthidin and ouabain was transient and returned to above the resting level while the muscle fibres were still exposed to these agents. 3. Recovery of membrane potential in cells exposed to anoxia is biphasic. An initial ‘fast’ phase of recovery occurs within 15 s upon return to air followed by a late ‘slow’ phase lasting several minutes. Recovery of input resistance in cells exposed to N2 coincided with the ‘fast’ phase of the recovery of resting membrane potential. 4. Recovery of membrane potential following exposure to strophanthidin is a long, slow process which occurs at conductance values at the resting level or below. 5. The tendency towards spontaneous action potentials was increased by anoxia and the action potentials occurring in anoxia were elongated into plateau potentials of about 18s duration. 6. These results are consistent with the hypothesis that anoxia and cardioactive steroids inhibit a metabolic process, possibly an electrogenic ion pump, that is essential for maintenance of the resting membrane potential in Drosophila flight muscle. Exposure to these agents also results in changes in input resistance. Both of these effects could contribute to the depolarization and affect the excitable properties of the muscle fibre membrane.

Effect of low chloride on relaxation in hamster diaphragm muscle

1986 ◽  
Vol 61 (1) ◽  
pp. 180-184 ◽  
Author(s):  
S. A. Esau ◽  
N. Sperelakis
Keyword(s):  
Membrane Potential ◽  
Muscle Fatigue ◽  
Time Constant ◽  
Diaphragm Muscle ◽  
Resting Membrane Potential ◽  
Krebs Solution ◽  
Sarcolemmal Membrane ◽  
Cl Conductance

With muscle fatigue the chloride (Cl-) conductance of the sarcolemmal membrane decreases. The role of lowered Cl- conductance in the prolongation of relaxation seen with fatigue was studied in isolated hamster diaphragm strips. The muscles were studied in either a Krebs solution or a low Cl- solution in which half of the NaCl was replaced by Na-gluconate. Short tetanic contractions were produced by a 160-ms train of 0.2-ms pulses at 60 Hz from which tension (T) and the time constant of relaxation were measured. Resting membrane potential (Em) was measured using KCl-filled microelectrodes with resistances of 15–20 M omega. Mild fatigue (20% fall in tension) was induced by 24–25 tetanic contractions at the rate of 2/s. There was no difference in Em or T in the two solutions, either initially or with fatigue. The time constant of relaxation was greater in low Cl- solution, both initially (22 +/- 3 vs. 18 +/- 5 ms, mean +/- SD, P less than 0.05) and with fatigue (51 +/- 18 vs. 26 +/- 7 ms, P less than 0.005). Lowering of sarcolemmal membrane Cl- conductance appears to play a role in the slowing of relaxation of hamster diaphragm muscle seen with fatigue.

Calcium channels and excitation–contraction coupling in cardiac cells. I. Two components of contraction in guinea-pig papillary muscle

1987 ◽  
Vol 65 (9) ◽  
pp. 1821-1831 ◽  
Author(s):  
E. Honoré ◽  
M. M. Adamantidis ◽  
B. A. Dupuis ◽  
C. E. Challice ◽  
P. Guilbault
Keyword(s):  
Membrane Potential ◽  
Guinea Pig ◽  
Papillary Muscle ◽  
Cardiac Cells ◽  
Resting Membrane Potential ◽  
Tonic Component ◽  
Contraction Coupling ◽  
Rich Solution ◽  
The Relationship ◽  
Guinea Pig Atria

Biphasic contractions have been obtained in guinea-pig papillary muscle by inducing partial depolarization in K+-rich solution (17 mM) containing 0.3 μM isoproterenol; whereas in guinea-pig atria, the same conditions led to monophasic contractions corresponding to the first component of contraction in papillary muscle. The relationships between the amplitude of the two components of the biphasic contraction and the resting membrane potential were sigmoidal curves. The first component of contraction was inactivated for membrane potentials less positive than those for the second component. In Na+-low solution (25 mM), biphasic contraction became monophasic subsequent to the loss of the second component, but tetraethylammonium unmasked the second component of contraction. The relationship between the amplitude of the first component of contraction and the logarithm of extracellular Ca2+ concentration was complex, whereas for the second component it was linear. When Ca2+ ions were replaced by Sr2+ ions, only the second component of contraction was observed. It is suggested that the first component of contraction may be triggered by a Ca2+ release from sarcoplasmic reticulum, induced by the fast inward Ca2+ current and (or) by the depolarization. The second component of contraction may be due to a direct activation of contractile proteins by Ca2+ entering the cell along with the slow inward Ca2+ current and diffusing through the sarcoplasm. These results do not exclude the existence of a third "tonic" component, which could possibly be mixed with the second component of contraction.

Sign in / Sign up

Export Citation Format

Share Document