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A I Solov'ev

Publications and source records attributed to A I Solov'ev.

At least 19 recordsLinked to original sources
PubMed1989

[Cellular mechanisms of transitory smooth muscle contraction of the coronary arteries during hypoxia: role of intracellular Ca2+].

In experiments on isolated porcine and canine coronary artery rings it was shown that vascular smooth muscle (VSM) during hypoxia (decreasing bath PO2 with 147 to 20-15 mm Hg) response to biphasic constriction-dilation reaction. Transient hypoxic contractions (THC) of VSM preserved completely in Ca2+-free solution and partially (up 50-60%) in the presence of Ca2+-channel blockers, but abolished by procaine. THC of VSM skinned by saponin significantly depressed at depletion of Ca2+-store sarcoplasmic reticulum (SR) by caffeine nd abolished after SR destruction. THC is not linked with Na+-K+-ATPase inhibition because it preserved (or increased) at ouabain treatment. THC significantly depressed under selective glycolysis blockade by monoiodoacetic acid and pyruvate and also after inositol-1 monophosphatase inhibition by lithium (the phase of hypoxic relaxation of VSM was augmented in this condition). Our results indicate that transient contraction of coronary arteries under hypoxia may be mediated mainly by release of Ca2+ from SR and linked obviously with production of inositol-1,4,5-trisphosphate. The participation of glycolysis in this process is unknown.

Animals↗
PubMed1988

[Cellular mechanisms of hypoxic coronary spasm].

Transient hypoxic contraction (THC) of vascular smooth muscle (VSM) of isolated human, canine and porcine coronary artery rings was preserved in Ca2+--free solution and abolished with procaine. The data obtained suggest that the THC of the coronary VSM is mediated via a Ca2+ release from sarcoplasmic reticulum under the effect of inositol-1,4, 5-triphosphate and may be triggered by action of endogenous noradrenaline on alpha 1-adrenoceptors. The mechanism of beta-adrenergic relaxation was not actualized in the hypoxia because of uncoupling of the beta-adrenoceptors from adenylate cyclase.

Animals↗
PubMed1988

[Magnesium ions and contractile activity of vascular smooth muscle cells in hypoxia].

In isolated smooth muscle of the rat portal vein removal of Mg2+ from perfusate induced rapid enhancement of frequency and amplitude of spontaneous contractions and decreased inhibiting effect of hypoxia on the smooth muscle contractile activity. Concomitant elevation of extracellular Ca2+ has no additional protective effect on the smooth muscle in hypoxia. Ten-fold lowering of Mg2+ content in buffer solution resulted in a significant rise in the tension of the smooth muscle activated by Ca2+. The data obtained suggest that protective effect of Mg2+-free solution on vascular smooth muscle in hypoxia may be mediated not only through increases intracellular Ca2+ concentration but also due to rising sensitivity of the smooth muscle cells contractile protein to Ca2+.

Animals↗
PubMed1986

[Role of the endothelium in the development of the contractile reactions of vascular smooth muscle during decreased oxygenation].

Noradrenaline-preactivated vascular smooth muscles (VSM) of the rat thoracic aorta showed two-phase reactions in response to decreased oxygenation: significant relaxation was preceded by transient constriction. When the endothelium was removed only VSM relaxation phase was retained, with no constriction observed. The data obtained suggest an endothelium-dependent nature of VSM constriction reaction to hypoxia, in contrast to endothelium-independent VSM relaxation. Intracellular calcium is also assumed to play an essential role in the formation of endothelium-dependent constriction VSM reaction to hypoxia.

Acetylcholine↗
PubMed1985

[Mechanism of changes in the calcium permeability of the sarcolemma of vascular smooth muscle cells during hypoxia].

In isolated preparations of smooth muscle of the rat portal vein, removal of Ca2+ from perfusate or addition of Ca2+--antagonists as well as hypoxia entailed inhibition of vascular smooth muscle contractile activity. Uptake of 45Ca by vascular smooth muscle cells was diminished in hypoxia. Liposomes filled with Ca2+ or Cr but not ATP prevented the hypoxic relaxation of vascular smooth muscle. One of the main reasons of the decrease of vascular smooth muscle contractility in hypoxia seems to be the disturbance of calcium channel phosphorylation and the decrease of sarcolemma calcium permeability.

Adenosine Triphosphate↗
PubMed1982

[Effect of a glycolysis block in the vascular wall on the phasic activity of smooth muscles].

A study was made of contractile reactions of spontaneously active smooth muscles of the portal vein during selective inhibition of glycolysis. Use was made of monoiodoacetate to inhibit first phasic and then tonic contractions of the vascular smooth muscles (VSM). Combined use of monoiodoacetate and pyruvate selectively inhibited phasic activity alone. A hypothesis is advanced as to the role played by the glycolytic oscillator as the triggering mechanism by which rhythmic phasic contractile activity is formed.

Animals↗
PubMed1981

[Effect of restricted oxygenation of vascular smooth muscles on the contractile effects of direct electrical and mechanical stimulation].

Contractility reactions of the smooth muscles of the rat portal vein and the umbilical vein of man to direct electrical stimulation and rapid stretch were examined under different PO2 levels in perfusate. It was shown that during perfusion of vascular preparations with oxygenated Krebs solution, the active myogenic responses to rapid stretch and contractility reactions to electrical stimulation are well pronounced and dependent on the stimulation intensity. The decrease in perfusate PO2 is accompanied by a considerably less increment of the amplitude of spontaneous contractions and tonic tension of the smooth muscles in response to direct mechanical and electrical stimulation, respectively. The data obtained allow a suggestion that physiological variation of the PO2 level may influence the reactivity and myogenic activity of the vascular smooth muscles and that this mechanism may participate in the local blood flow control and correction of central neurogenic effects.

Animals↗
PubMedDate not supplied

[Characteristics of the contractile reactions of rhythmically active vascular smooth muscles in spontaneously hypertensive rats undergoing hyperoxygenation and the role of the endothelium in their development].

Experiments on isolated preparations of the portal vein from healthy and spontaneously hypertensive rats have revealed that removal of the endothelium has no influence on hyperoxygenation-induced increase in the contractile activity of vascular smooth muscles (VSM). It is also shown that VSM from hypertensive rats demonstrate higher sensitivity to hyperoxygenation than VSM from healthy rats. Results of the study confirm a supposition that contractile effect of hyperoxygenation on VSM is realized mainly via direct influence of oxygen on plasma membranes of VSM and increase of the membrane permeability for extracellular Ca2+.

Animals↗