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Biomedical subjects

M F Shuba

Publications and source records attributed to M F Shuba.

At least 73 records · Page 4Linked to original sources
PubMed1981

[Mechanism of the relaxant action of noradrenaline on coronary artery smooth muscle cells].

Electrical and contractile activity of smooth muscle cells (SMC) of bovine coronary arteries was examined by the double sucrose gap method. It was shown that, on the one hand, noradrenaline increased the potassium membrane permeability followed by hyperpolarization which led to the closing of potential-dependent show calcium channels and to the reduction of the transmembrane calcium ion influx. On the other hand, noradrenaline closed potential-dependent chemosensitive calcium channels that limited influx of extracellular calcium ions into SMC. Such a double-noradrenaline effect resulted in a considerable decrease of the concentration of intracellular calcium ions and in the falling of the basal tone of arterial SMC.

Animals↗
PubMed1980

[Effect of potassium ions on electrogenesis and contraction of ureter smooth muscle].

In the ureter smooth muscle cells, high--K solution produced a depolarization at the onset of which the action potentials (AP) and contraction occur; the latter consists of an initial phasic (Ph) and subsequent tonic (T) components. Ph component is initiated by the AP, T component--by a stable potassium depolarization. In Ca--free solution the AP, Ph and T components are blocked, although a sustained potassium depolarization is preserved. Basing on these results it is suggested that: 1) phasic contraction is initiated by calcium ions influxed via fast potential--dependent calcium channels participating in the AP generation; 2) tonic contraction is also initiated mainly by extracellular calcium influx through slow potential--dependent calcium channels of plasmatic membrane that appear to be similar to calcium channels of sarcoplasmic reticulum membrane in skeletal muscles and of the membrane of presinaptic nerve terminals.

Action Potentials↗
PubMed1980

[Effect of manganese ions and verapamil on electrogenesis and contraction of ureter smooth muscle].

Fast and slow calcium channels of the electrically excitable membrane of the ureter smooth muscle cells had different sensitivity to manganese ions and verapamil. Manganese ions (10(-4) M) selectively blocked the fast potential--dependent Ca--channels, Ca ions being necessary for phasic contraction, whereas verapamil (10(-9)--10(-8)) specifically blocked the slow potential--dependent CA--channels.

Action Potentials↗
PubMed1978

[Effect of strychnine, hydrastine and apamin on synaptic transmission in smooth muscle cells].

The effects of strychnine, hydrastine and apamine on nervemuscle transmission in guinea pig stomach and taenia coli were studied. Hydrastine and strychnine produced an increase in non-adrenergic IPSPs of smooth muscle cells. Under apamine action IPSPs and hyperpolarization caused by exogenous ATP were reversibly blocked and non-cholinergic EPSPs appeared. ATP caused depolarization of the cell membrane in this condition. Consequently, apamine is a specific (postsynaptic) blocking agent of non-adrenergic inhibition and ATP obviously mediates both non-adrenergic inhibition and non-cholinergic synaptic excitation of smooth muscle cells observed in our experiments.

Adenosine Triphosphate↗
PubMed1978

[Selective inhibition of the tonic component of portal vein smooth muscle cell potassium contracture by verapamil].

The studies were performed on the rat portal vein smooth muscle cells, using double sucrose-gap method. 10(-9)--10(-7) M-verapamil was shown to selectively block the tonic component of potassium contracture. Since potassium depolarization of the membrane persists, it may evidence that verapramil had a specific effect on the excitation-contraction coupling by blocking the passive calcium entry into the muscle cells. At higher concentrations (10(-6)--10(-5) M) verapramil produced inhibition of the phasic component of potassium contracture by blocking the potential-dependent calcium canals of the portal vein smooth muscle cell membrane responsible for generation of the action potentials.

Action Potentials↗
PubMed1977

The effect of sodium-free and potassium-free solutions, ionic current inhibitors and ouabain on electrophysiological properties of smooth muscle of guinea-pig ureter.

1. The effects of Na-free and K-free solutions, tetraethyl ammonium (TEA), Mn2+, verapamil and ouabain on the electrophysiological properties of the smooth muscle cells of guinea-pig ureter have been studied, using the double sucrose-gap method. 2. TEA (5 mM) increased the amplitude and duration of both the initial spike component and the subsequent plateau of the action potential. The repetitive spike discharge on the plateau was abolished. The amplitude and duration of the phasic contraction was increased. The threshold for excitation was lowered while the resting potential and membrane resistance were unaffected. 3. In Na-free solution the duration of the action potential decreased mainly due to the suppression of the plateau. A similar effect was produced by exposure to K-free solution and also by ouabain. 4. Mn2+ (2 mM) suppressed the spike component and raised the threshold for excitation. The amplitude of the remaining part of the action potential was markedly increased but the contraction was rapidly abolished. The resting potential and membrane resistance were unchanged. When Mn2+ was added to Na-free solution it produced an increase in the amplitude and duration of the remaining part of the action potential but the phasic contraction was abolished. 5. Verapamil did not specifically block the fast component of the action potential but initially increased the amplitude of the spike and shortened the plateau. Subsequently, both the action potential and the phasic contraction became smaller. 6. The observations indicate that the phasic contractions are triggered by the initial spike component of the action potential, whereas the plateau is associated with the amplitude and particularly the duration of the contraction.

Action Potentials↗
PubMed1977

The mechanism of the excitatory action of catecholamines and histamine on the smooth muscle of guinea-pig ureter.

1. The ionic mechanism of the excitatory action of catecholamines and histamine on the smooth muscle cells of guinea-pig ureter was studied with the double sucrose-gap method. 2. In normal conditions adrenaline and noradrenaline in a concentration of 10(-5) g/ml., and histamine in a concentration of 10(-6) g/ml., prolonged the duration of the plateau of the action potential and increased the amplitude and duration of the phasic contraction. Sometimes these changes were accompanied by a slight depolarization of the muscle membrane and by a small increase (with noradrenaline) or decrease (with histamine) of the membrane resistance. The amplitude and duration of the fast spike component of the action potential were not changed. 3. Isoprenaline in a concentration of 10(-5) g/ml. either caused no change or it decreased the duration of the plateau, reduced the amplitude of contractions and reduced excitability. 4. Tetraethyl ammonium (TEA; 5 mM), which blocks the delayed outward K current, did not prevent the increase in the duration of the plateau nor the increase of the amplitude and duration of the contractions by noradrenaline and histamine. 5. In Na-free or in K-free solution or in the presence of ouabain, i.e. in conditions in which the Na-gradient across the membrane was reduced, noradrenaline and histamine were unable to increase the duration of the plateau and the amplitude and duration of the contraction. 6. In the presence of Mn2+ (2 mM) which suppressed the spike component of tha action potential and the phasic contraction, theeffects of noradrenaline and histamine were almost abolished. 7. The results suggest a dual ionic mechanism of the alpha-action of catecholamines and of the action of histamine on the smooth muscle of ureter: (1) these drugs affect the passive ionic permeability of the membrane in a manner that results in depolarization; (2) they specifically activate the potential-dependent conductance of the slow Na channels, thereby increasing the plateau duration. The increased amplitude and duration of the contraction is the result of their primary effect on the plateau of the action potential.

Action Potentials↗