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Biomedical subjects

V A Buryĭ

Publications and source records attributed to V A Buryĭ.

At least 19 recordsLinked to original sources
PubMed1992

[Effects of the membrane potential level on serotonin-induced contraction of the pulmonary artery smooth muscle in rabbits].

The effects of changes in membrane potential level on the electrical and contractile responses induced by serotonin (10(-6) mol/l) were investigated in muscle strips from rabbit main pulmonary artery using sucrose-gap technique. In spite of the fact that serotonin-induced depolarization did not exceed the threshold level for development of contraction, it was followed by a strong tonic contraction. Nearly a half of this contraction could be relaxed by an electrotonic hyperpolarization of the membrane. A week preliminary depolarization of the muscle cells resulted in an increase while a strong depolarization--in dramatic decrease of serotonin-induced contraction. Nifedipine effectively blocked potassium-induced, but not serotonin induced contraction. We suggest that in addition to voltage-operated and receptor operated Ca channels in vascular smooth muscle cell membrane there is a separate class of nifedipine-insensitive Ca channels operated by both serotonin receptor and membrane potential.

Animals↗
PubMed1988

[Membrane mechanisms of the excitatory action of serotonin on the smooth muscles of the rabbit pulmonary artery].

Serotonin induced dose-dependent tonic contractions of the rabbit pulmonary artery smooth muscles with KED50, of 2.7 X 10(-7) mol/l. More than 80% of these contractions were found to be dependent on extracellular calcium. Hyperpolarization of cell membrane by inwardly applied electrical current caused nearly 50% reduction in serotonin-induced contractions. The same portion of contractions was inhibited by verapamil and Ca2+. Serotonin-, but not potassium-induced contractions were completely inhibited by sodium nitroprusside which is thought to be selective inhibitor of receptor-operated calcium channels. These findings could indicate that Ca2+ ions, responsible for serotonin-induced contractions enter the cell from the outer surface of the cellular membrane via receptor-operated calcium channels. Nearly half of serotonin-operated Ca2+ channels appear to be also potential-operated.

Animals↗
PubMed1988

[The role of intra- and extracellular Ca in the activation of contraction of pulmonary artery smooth muscles induced by serotonin].

In Ca-free EGTA-containing solution serotonin induced a transient contraction of rabbit pulmonary artery smooth muscle which decayed to nearly steady-state level accounted for 17.7 +/- 1.6% of original contraction in Krebs solution. Both phasic and tonic components of this contraction were effectively inhibited by verapamil and Cd2+. Caffeine induced no contraction of muscle strips if it was applied after withdrawal of serotonin. But when the sequence of these drugs application was reversed, serotonin still evoked contraction with reduced phasic component. The results obtained in these experiments suggest, that serotonin-induced contraction of pulmonary artery smooth muscle is partly (less than 20%) due to mobilization of bound calcium from at least two stores located on the opposite sides of the cell membrane. Calcium released from external store site enters the cell via receptor-operated calcium channels.

Animals↗
PubMed1987

[Electrophysiological analysis of the action of kavinton on the smooth muscles].

Cavinton at a concentration of 10(-7)-10(-5) M was found to have a dose-dependent relaxing effect on bovine cerebral artery smooth muscles, without changing the resting potential and membrane resistance. Smooth muscles of the rabbit portal vein and guinea-pig taenia coli were insensitive to low cavinton concentrations. The results are consistent with the hypothesis that relaxing action of cavinton is due to the blocking of Ca2+ ions influx into the cells of cerebral artery through receptor-operated calcium channels. At higher concentrations (exceeding 10(-5) M) cavinton exerts nonspecific influence on the smooth muscles under study, inhibiting their excitability and decreasing membrane resistance resulting in the attenuation of tetanic contractions in the smooth muscles of the portal vein and taenia coli.

Animals↗
PubMed1986

[Electrical properties and transmembrane ion currents of single smooth-muscle cells].

Current and voltage clamp investigations of freshly isolated smooth muscle cells from guinea-pig ileum and taenia coli were performed using single suction micropipette technique. Specific membrane capacity of smooth muscle cells was calculated and accounted for 1.6 microF/cm2, with specific resistance varying from 50 to 150 k omega X cm2. Transmembrane currents consisted of two inward components, inactivating and noninactivating ones, carried by Ca2+ ions, overlapping with early activated potassium outward current. Time constant of inward current activation was not only voltage-sensitive but also ion-dependent. When Ca2+ ions in Krebs solution were replaced by Ba2+, both the rate of activation and inactivation of inward current were significantly reduced. Estimation of intracellular Ca2+ concentration increase has indicated that inward calcium current transports enough Ca2+ for direct contraction activation.

Animals↗
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↗
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↗
PubMed1980

[Transmembrane ion currents in pulmonary artery smooth muscle].

Transmembrane ionic currents were investigated in the rabbit pulmonary artery smooth muscle under voltage clamp conditions with the use of the double sucrose gap method. With depolarizing pulses, there developed a fast inactivated outward current that was followed by a steady-state outward current. Tetraethylammonium (TEA) partly suppressed the outward current, and the fast inward current that preceded the fast outward one could be seen in these conditions. Appearance of the fast inward current in TEA-containing solution suggests the overlapping of the fast inward and outward currents. It appears that the resultant transmembrane current has an outward direction since in normal conditions the permeability of the fast potassium channels exceeds that of calcium channels. Conditioning hyperpolarization increased and depolarization decreased the fast outward current indicating that at the resting membrane potential a part of the potassium channels is inactivated and this inactivation is removed by hyperpolarization.

Animals↗
PubMedDate not supplied

[The role of calcium and potassium conductance in electrogenesis of smooth-muscle cells of the basilar artery].

The role of calcium and potassium conductances in electrogenesis of smooth muscle cells of the bovine basilar artery has been investigated using blocking agents of calcium and potassium channels both in the normal Krebs solution and in hyperpotassium solution under anelectrotonic repolarization of the cell membrane. It is shown that both voltage-operated calcium and potassium conductances participate in generation of gradual action potentials evoked by electrical stimulation. A higher contribution of potassium conductance into the total membrane conductance during depolarization is found to be the main factor interfered with development of full-size action potential.

Action Potentials↗