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Biomedical subjects

M F Shuba

Publications and source records attributed to M F Shuba.

At least 55 records · Page 3Linked to original sources
PubMed1986

[Electrophysiological research on the coupling of excitation-contraction during alpha-adrenoreceptor activation in blood vessel smooth muscles].

Alpha 1-adrenoceptor blocker--prazosin--was found to inhibit noradrenaline-induced depolarization and concentration in the smooth muscles of the portal rabbit vein, indicating that this reaction was due to alpha 1-adrenoceptor activation. In the pulmonary artery both alpha 1 and alpha 2-adrenoceptors appear to be involved in noradrenaline excitatory action, as the effect was not completely inhibited by prazosin. The results suggest that hypotensive action of prazosin is related to the cessation of Ca2+ ion influx through alpha 1-operated calcium channels. The decrease in Ca2+ influx through voltage-dependent calcium channels due to prazosin-evoked elimination of depolarization can also contribute to this effect.

Action Potentials↗
PubMed1986

[Nature of non-adrenergic inhibition in the smooth muscles of the human intestine].

Electrical responses of longitudinal and circular smooth muscles of human small intestine and colon to ATP, alpha, beta-methylene-ATP, beta, gamma-methylene-ATP and adenosine were studied by the sucrose-gap method. In most cases ATP induced the effect similar to that of stimulation of the nonadrenergic inhibitory nerves. Desensitization of the purinergic receptors by alpha, beta-methylene-ATP selectively decreased the amplitude of inhibitory junction potentials. The results confirm the purinergic hypothesis of the nonadrenergic inhibition in human intestine.

Adenosine↗
PubMed1985

Possible mechanism of adrenergic and nonadrenergic inhibition in intestinal smooth muscle cells.

Nonadrenergic synaptic transmission in circular and longitudinal smooth muscles of caecum preexposed to K-free solution for 4-5 h has been studied by means of sucrose gap technique. In addition, the effects of noradrenaline (NA) and ATP on these muscles were investigated under these conditions. The action of the above substances was accompanied by depolarization and contraction. NA induced a decrease in the membrane resistance. Addition of 0.5 mM Ba2+ to K-free solution intensified the depolarization. 1 mM of Mn2+ blocked depolarization and contraction. Intramural stimulation produced noncholinergic e.j.p.s blocked by TTX. Addition of 0.5 mM Ba2+ increased their amplitude. A reversal potential of both NA-induced depolarization and e.j.p. was in the range of + 10 to + 20 mV. It is supposed that e.j.p.s and depolarization observed in response to ATP and NA action are due to an increase in calcium permeability of the membrane.

Adenosine Triphosphate↗
PubMed1985

[Calcium current and electromechanical coupling in the smooth muscle cells of the stomach].

The relationship between inward current and contraction was studied with double sucrose gap technique and measurement of contraction of the small muscular bundle in circular muscle from the fundus of guinea pig stomach. In voltage-clamped circular muscle, an inward current observed during depolarizing potential step was sensitive to Cd2+ or low external Ca2+ and had two components: a transient and a steady-state ones. Inactivation of this current was both voltage-dependent and Ca-current-dependent. Transient inward current activated phasic contraction, while the steady-state current activated tonic contraction. The voltage--dependence of the steady-state inward current was estimated with the Hodgkin--Huxley equation.

Animals↗
PubMed1984

[Synaptic processes in smooth muscles].

Junction potentials evoked by intramural stimulation were investigated in smooth muscles of guinea-pig gastrointestinal tract by means of intracellular recording and sucrose-gap methods. It was shown that cholinergic nerve-muscle transmission is only excitatory and more effective in fundic smooth muscles as compared with other part of the gut. Adrenergic nerve control of gastrointestinal motility is carried out both by excitation and inhibition of the smooth muscles. Nonadrenergic inhibition was observed in circular muscle layer of all parts of the gut and was more effective in distal colon. Noncholinergic, nonadrenergic excitation in caecum smooth muscles is shown to be of complex nature. It consists of an initial excitatory junction potential followed by a slow late wave of depolarization. In other parts of the gastrointestinal tract such an excitation is manifested only by a slow late wave of depolarization.

Adrenergic Fibers↗
PubMed1983

[Effect of adenosine and ATP on electrogenesis and contraction in the smooth muscles of the cerebral arteries].

The effects of adenosine and ATP on electrogenesis and contraction in smooth muscles of the cattle basilar and middle cerebral arteries was studied with a modified sucrose gap technique. Adenosine (10(-8) - 10(-3) M) and ATP (10(-8) - 10(-6) M) induced relaxation of the muscle strips with no change in resting potential of the muscle cells. ATP (10(-5) - 10(-3) M) led to depolarization of the cell membrane followed by a hyperpolarization which was accompanied by the complex contractile reaction of muscle strips. Adenosine (10(-3) M) caused relaxation comparable to the relaxation induced by Ca++-free solution or by Mn++ ions. This suggests that extracellular Ca++ ions which participate in maintaining of the blood vessel tone enter the smooth muscle cells mainly through the stationary open adenosinesensitive Ca channels of the membrane. Ca++ ions entering the smooth muscle cells through voltage-dependent noninactivating Ca channels contribute to maintaining of cerebral arteries' basal tone. Adenosine does not affect the voltage-dependent influx of extracellular Ca++ ions through the slow noninactivating Ca channels of the cell membrane or through fast inactivating Ca channels, participating in the AP generation.

Adenosine↗
PubMed1983

[Nature of electromechanical connections in the smooth muscle cells of the pulmonary artery].

Depolarization of the rabbit pulmonary artery smooth muscle cells over critical level (5-7 mV) by outward current or high K+ solution application produced contraction proportional to the depolarization. High K+ solution produced an initial spike on the rising phase of depolarization followed by subsequent phasic contraction amplitude of which was lower than that of the tonic one. Anelectrotonic repolarization of smooth muscle cells by means of inward current in high K+ solution was usually followed by spontaneous AP generation and subsequent phasic contractions which were summed and increased total contractile tension. If the spontaneous APs were not generated anelectrotonic repolarization was followed by relaxation of the smooth muscle proportional to the extent of repolarization. AP in this case could be evoked by electrical stimulation. Experiments with Ca--free solution and application of Ca and K-channel blockers suggest the existence of two types of voltage--dependent Ca--channels in the membrane of these smooth muscle cells: fast inactivated responsible for AP generation and phasic contraction, and slow noninactivated responsible for tonic contractions, dependent on the transmembrane potential. In physiological conditions, a functional role of the fast Ca channels is limited due to early activation of K-conductance which is comparatively large in these smooth muscle cells and suppresses AP generation.

Action Potentials↗
PubMed1983

[Properties of synaptic currents during non-adrenergic inhibition of the smooth muscle cells of the large intestine in the guinea pig].

Inhibitory junctional currents (IJCs) were recorded under voltage clamp conditions in response to brief transmural stimulation of the circular muscle of the guinea pig colon using the double sucrose gap method in the presence of atropine. The time course of IJC decay was approximately exponential 100-150 ms after the peak value. The IJC amplitude depended linearly on the membrane potential with the reversal potential (-70 mV) near the potassium equilibrium potential. The time constant (tau) of the IJC decay depended exponentially on the membrane potential and became e-fold decreased when the membrane was hyperpolarized approximately by 120 mV. Varying the quantal content of IJC caused an increase of tau upon rising the amount or transmitter released and its decrease with the depression of IJC. Application of ATP (10(-3)M) caused a decrease of tau and IJC amplitude, while apamine reduced the amplitude of IJC without any changes in their time course. The results are discussed in terms of a buffered diffusion hypothesis supposing a cooperative action of transmitter released on junctional receptors.

Adenosine Triphosphate↗
PubMed1982

[Excitation-contraction coupling in the smooth muscle cells of the portal vein as affected by noradrenaline].

Verapamil (10(-5) M) blocked phasic and tonic components of potassium contracture of smooth muscle cells (SMC) of the rat portal vein but failed to block completely noradrenaline, induced contraction of these cells, neither did it suppress the NA-induced contraction of the portal vein SMC in the presence of potassium contracture. These data suggest that NA-induced contraction is activated by external Ca2+ ions entering the SMC through chemosensitive (NA) voltage-independent Ca channels of the membrane. The contraction blocked by verapamil is activated by external Ca2+ ions entering through fast voltage-dependent inactivating Ca channels participating in AP generation, and slow voltage-dependent inactivating Ca channels opened by NA depolarization. The basal tone and contraction evoked by transmitters and physiologically active substances in the SMC of all blood vessels seem to be activated primarily by external Ca2+ entering the SMC via the above mentioned types of Ca channels.

Action Potentials↗
PubMed1982

[Electrogenesis and contraction of smooth muscle taenia coli kept in a solution with elevated concentration of potassium ions].

Experiments performed on smooth muscle strips of guinea-pig taenia coli in high-potassium solution using sucrose-gap method revealed that phasic and tonic components of contractile response following potassium depolarization were due to influx into the cells of Ca++ ions from extracellular solution through two types of voltage-dependent Ca channels: the fast inactivated and the slow noninactivated those. After cessation of the fast Ca channel inactivation with anodal current the membrane recovers its ability to generate spontaneous or evoked AP depending on repolarization level. Under these conditions AP generation can also occur in Ca-free and Na-free solutions due to regenerative process of K-channel activation.

Action Potentials↗
PubMed1982

[Mechanism of modulating effect of histamine on the excitation and contraction of smooth muscles of the ureter].

Experiments were carried out on smooth muscle cells (SMC) of the guinea-pig ureter by the double sucrose gap method with simultaneous recording of electrical and contractile activities. The effect of histamine on SMC was studied in normal Krebs solution and in sodium-free Krebs solution with TEA. In normal Krebs solution, histamine was shown to increase the duration of AP plateau and contraction. In sodium-free Krebs solution with TEA, the APs of ureter SMC also had a plateau that was determined by the increased calcium conduction of the membrane. In these conditions, histamine provoked a decrease in the duration of the AP plateau and contraction. The histamine effect was blocked by phencarol both in normal and sodium-free Krebs solution with TEA. A possible role of sodium, calcium and potassium ions in the modulating action of histamine on excitation of ureter SMC is discussed.

Action Potentials↗