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Biomedical subjects

V M Taranenko

Publications and source records attributed to V M Taranenko.

At least 19 recordsLinked to original sources
PubMed1990

[The dynamic changes in the functional characteristics of the vascular endothelium and smooth muscle cells under conditions of long-term hypercholesterolemia].

The course of the rabbit aortic wall reactivity changes due to hypercholesterolemia involved, in the first place, the inhibition of the endothelium relaxing influence on the smooth muscle contractile activity and an increase in the muscle sensitivity to neurogenic and humoral tonic influences. Later, a sharp inhibition of the vessel's wall functional activity occurred due to a mechanical factor: the development of connective tissue which prevents active vascular reactions. Nevertheless, endothelial and smooth muscle cells functional activity was high enough. The main cause of the vascular reactivity disturbances involved structural changes in the vessel wall whilst the direct influence of high blood cholesterol was much less obvious.

Acetylcholine↗
PubMed1989

[Effects of hypercholesterolemia on the electrical and contractile properties of the blood vessel wall].

The investigations were performed on the ring strips of rabbit aorta. The electrical activity of the vessels smooth muscle cells was registered by the "sucrose gap" method; the contractile activity of the strips was determined simultaneously. Experimental atherosclerosis was induced by keeping rabbits on a special diet enriched by cholesterol for 2 and 4 months. Strips were prepared with intact or mechanically removed endothelium. Hypercholesterolemia was shown to inhibit the reactivity of the vessel's wall to the weakening action of acetylcholine due to endothelial stimulation. The cause of these changes was the inhibition of the endothelial functional activity and inactivation of mechanisms by which endothelium influences smooth muscle cells.

Acetylcholine↗
PubMed1988

[Ionic mechanisms of endothelium-dependent relaxation of vascular smooth muscle under the action of acetylcholine].

Acetylcholine and nitroglycerin were shown to induce relaxation in muscles of the ring vascular segments of canine coronary arteries and rabbit aortic archs, the magnitude of the reaction depending on the level of initial tonic tension. Methylene blue abolished the relaxation. Mechanical removal of endothelium abolished the reaction to acetylcholine but not to nitroglycerin. Verapamil decreased the relaxation by 70%. The endothelium-dependent relaxation seems to be connected mainly with a decrease in the calcium entering vascular smooth muscle cells through voltage-dependent channels.

Acetylcholine↗
PubMed1987

[Mechanism of activation of contraction of smooth muscle cells of coronary arteries induced by acetylcholine].

Acetylcholine (ACh) caused a slight depolarization, decrease of the membrane resistance and tonic contraction of the circular muscle strips from bovine coronary arteries. On removal of Ca2+ ions by adding EGTA and Mg2+ ions, a drop in basal tone was observed, as well as the decrease of the membrane resistance and a considerable reduction of the SMC contractile reaction (by 90% from normal value) in response to ACh. In presence of verapamil, ACh also caused contraction which, however, was half of that in normal conditions. In the course of potassium depolarization, ACh produced contraction of the strip, the maximal decrease of contraction being observed at 80 mM potassium depolarization. The ACh-induced contraction of coronary arteries seems to be activated mainly by extracellular calcium ions.

Acetylcholine↗
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↗
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

[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↗
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↗
PubMed1980

[Coupling of electrical processes on the membrane to the contractile activity of anococcygeus smooth muscle cells].

Rabbit anococcygeus smooth muscle cells (SMC) were studied by means of the double saccharose bridge method. The contractile apparatus of anococcygeus SMC was shown to be activated by two ways: by action potentials (AP) and by steady depolarization of the membrane potential. In view of the fact that calcium current blockers (Mn2+ and Cd2+) inhibit APs and phasic contractions, APs of SMC have calcium nature and phasic contractions are evoked by the same ions that are involved in AP generation and enter muscle cells via fast potential-dependent calcium channels. Since Cd2+ completely but reversibly blocks tonic contractions, it is assumed that the tonic component of contraction is also activated by extracellular calcium ions that enter muscle cells via so-called slow potential-dependent calcium channels activated by steady depolarization of muscle cells. Therefore, both phasic and tonic contractions in anococcygeus muscle cells are evoked largely by extracellular calcium ions.

Animals↗