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Biomedical subjects

V M Taranenko

Publications and source records attributed to V M Taranenko.

At least 37 records · Page 2Linked to original sources
PubMed1980

[Mechanisms of activation of coronary vessel smooth muscle contraction].

Experiments have been performed with smooth muscle cells (SMC) of the circular strips from the bovine left descending anterior heart artery with a diameter of 2--2.5 mm. Use was made of the double sucrose gap method with simultaneous recording of electric and contractile activity of SMC. The cathode of polarizing current produced depolarization of SMC membrane (cathelectrotone). After depolarization of the membrane reached the threshold, the action potential (AP) was generated, followed by SMC contraction. The anode of polarizing current caused hyperpolarization of the membrane (anelectrotone) accompanied by relaxation of the strip. The degree of relaxation depended upon the initial muscle tone and the magnitude of anelectrotonic hyperpolarization. The voltage-current characteristics of SMC show that the muscle cell membrane of the coronary arteries possesses pronounced rectifying properties. An increase in the external potassium concentration up to 160 mM results in depolarization of the SMC membrane preceded by AP. These changes are accompanied by initial phasic and subsequent tonic contraction. The phasic component of the contraction is suggested to be evoked by AP and tonic component by stable potassium depolarization.

Action Potentials↗
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

[Effect of increased calcium ion concentration on the electrical and contractile activity of guinea pig ureter smooth muscle].

Experiments were performed on the smooth muscle cells of the guinea pig ureter by means of the double sucrose-gap method. An increase of Ca2+ concentration (22 mM/1) in Ringer-Locke solution causes hyperpolarization and a slight increase of the membrane resistance. The amplitude of the first spike potential and the plateau decreases, the amplitude of oscillations increases. In sodium-free Ringer-Locke solution when the action potential in the smooth muscle cells of the ureter turns into a simple spike potential, an increase of Ca2+ concentration causes a marked increase of the action potential amplitude.

Action Potentials↗
PubMed1976

[Synaptic potentials in smooth muscle cells].

Investigations were carried out on smooth muscle cells (SMC) of rat and rabbit anococcygeus by the method of a double "sugar bridge" in the presence of tetraethylammonium (1 mM/1) in the Krebs solution. Stimulation of the muscle strip by the electric current rectangular pulse of the maximal value and of short duration caused the development of excitatory postsynaptic potentials (EP SP) in the rat and rabbit SMC, and of inhibitory postsynaptic potentials in the rabbit SMC. The value of postsynaptic potentials displayed a linear dependence on the level of the membrane potential. Elimination of chlorine ions from the external solution decreased the EP SP of the SMC of rabbit anococcygeus and shifted the reversion potential in the direction of sodium balance potential. Apparently generation of the EP SP of the SMC of rabbit anococcygeus was associated with the increased permeability of the membrane both for sodium and for chlorine ions.

Action Potentials↗
PubMedDate not supplied

[Character and mechanisms of changes in vascular wall reactivity in prolonged hypercholesterolemia].

Changes in the structure and functional properties of the vascular wall after 8 months of alimentary hypercholesterolemia (HCE) were studied. The experiments were conducted on the circular bands of the arch of the aorta in rabbits. Sharp inhibition of the reactivity of the vascular bands was established, which was associated first of all with thickening of the intima due to the development of fibro-atheromatous changes in it. At the same time, the smooth-muscle cells of the vascular wall maintained marked reactivity to various direct and receptor-mediated test effects. The functional significance of the endothelium in regulation of the vascular tonus, manifested by weakened endothelium-dependent relaxation, was sharply inhibited in the late stages of HCE. It is shown that reduction of the sensitivity of the smooth-muscle cells to the endothelium-dependent relaxation factor is the principal factor of weakening of the endothelium-dependent dilatational effects. After 8 months of HCE the aortic wall is capable of liberating a substance which is similar to the endothelium-dependent relaxation factor in its action, even when the thickened intima is completely removed.

Animals↗
PubMedDate not supplied

[Efficacy of vascular wall protection from atherosclerotic damage using various calcium antagonists].

The authors studied the effect of various calcium antagonists--verapamil (VP) and Mg2+ (MgCl2) on the character of affection of the vascular wall ulcer conditions of prolonged hypercholesterolemia (HCE). The blood cholesterol (CS) content increased by the end of the 8th month of HCE to eight-fold the value in intact animals. The specific atherosclerotic changes in this case occupied approximately 80% of the area of the thoracic aorta whose functional properties changed essentially. The values of constricting responses of bands to noradrenaline (NA) was 45% of that in intact rabbits, the dilatating responses to acetyl choline (AC) and nitroglycerin (NG) were 20% and 35% of those in intact animals, respectively. Combination of HCE with daily VP injection (1 mg) led to a decrease in the area of affection of the aorta by 20%, which hardly affected the severity of HCE. A slightly more pronounced than in animals only with HCE (controls) was the response of bands to NA, AC, and NG (by 5, 30, and 15%, respectively). The protective effect of MgCl2 (200 mg/kg) was more significant--the affected area of the thoracic aorta reduced by 50% as compared to the controls, the constricting response to NA was maintained at a level exceeding the control level by 25%, the dilatating responses to NG and AC exceeded the control values 2 and 1.5 times, respectively, on the average. The severity of HCE diminished by 50%. The results of the study indicate that the organic and, in particular, the inorganic blocking agents of the calcium canals possess a marked angioprotective action and may be applied for the prevention of vascular atherosclerosis.

Animals↗
PubMedDate not supplied

[Functional state and adrenergic reactivity of the myocardium in experimental atherosclerosis].

The authors studied the changes in the functional properties of a rabbit heart in protracted alimentary hypercholesterolemia (HCE). It is shown that HCE has a little effect on the characteristics of myocardial contractility and adrenergic sensitivity. In protracted HCE the probability of the occurrence of a myocardial own rhythm in response to the effect of isoprenaline increased. HCE with simultaneous vasopressin administration failed to change the contractile properties of the myocardium but had a marked effect on the adrenoreceptor apparatus. The sensitivity of muscles to isoprenaline and phenylephrine increased significantly. The possibility of the appearance of a myocardial own rhythm increased. The results of the study are indicative of the essential role of vasospasm in the development of atherosclerotic myocardial injuries.

Animals↗