[Two components of sodium-azide insensitive Mg2+,ATP-dependent Ca2+ transport in ureteral smooth muscle membrane structures]. / Dve komponenty nechuvstivitel' k deistviiu azida natriia Mg2+-,ATP- zavisimogo transporta Ca2+ v membrannykh strukturakh gladkoi myshtsy mochetochnika.

The effects of Ca(2+)-precipitating anions (oxalate and phosphate) and effective inhibitors of endo/sarcoplasmic reticulum calcium pump (thapsigargin and cyclopiazonic acid) on azide-insensitive (5 mM) Mg2+,ATP-dependent Ca2+ accumulation in microsomes of ureter smooth muscle cells were studied. Oxalate (0-20 mM) and phosphate (0-60 mM) stimulate Mg2+,ATP-dependent Ca2+ accumulation. Thapsigargin and cyclopiazonic acid at 100 nM and 20 microM, respectively, completely inhibited (i.e., down to the level in the absence of oxalate) Ca2+ accumulation activated by 10 nM oxalate. These inhibitors only partially inhibited Ca2+ accumulation activated by 40 mM phosphate. Mg2+,ATP-dependent Ca2+ accumulation in microsomes, which is inhibited by thapsigargin and cyclopiazonic acid and activated by oxalate or phosphate, can result from functioning of calcium pump in endoplasmic reticulum of ureter myocytes. The inhibition constant, Ki, was calculated by the method of Hill and it was 0.3 nM and 0.2 microM for thapsigargin or cyclopiazonic acid, respectively. Mg2+,ATP-dependent Ca2+ accumulation in microsomes, which is insensitive to thapsigargin or cyclopiazonic acid and activated by phosphate, can result from functioning of calcium pump in plasma membranes of ureter myocytes.

[The calcium pump in the sarcolemma controls smooth muscle relaxation]. / Kal'tsievyi nasos sarkolemmy kontroliruet rasslablenie gladkoi myshtsy.

In order to identify the functional role of the sarcolemma calcium pump in the control over smooth muscle relaxation there was studied the effect of temperature on relaxation kinetics of myometrium carbachol contracture, actomyosin superprecipitation isolated from this object and Mg2+, ATP-dependent transport of Ca2+ in the fraction of uterus sarcolemma vesicles. The activation energies of the processes under study were determined in comparison. It was concluded from the evidence obtained that relaxation of the smooth muscle contracture is controlled by the stimulated temperature increase and by Na(+)-independent trans-sarcolemma release of Ca2+ from the myocytes sensitive to La3+ effect. The release is provided by the calcium pump of the plasmic membrane.

[Uterotonic action of sigetin and its effect on the Mg2+, ATP-dependent transport and stationary metabolism of Ca2+ through the myometrial sarcolemma]. / Uterotonicheskoe deistvie sigetina i ego vliianie na Mg2+, ATP-zavisimyi transport i statsionarnyi obmen Ca2+ cherez sarkolemmu miometriia.

The effect of sigetin (dipotassium salt, meso-3, 4-di-(n-sulfophenyl)- hexane) on the electrical and mechanical activity, Ca2+, Mg2+-ATPase activity and Mg2+, ATP-dependent Ca2+ transport in uterine smooth muscle have been investigated. Sigetin caused depolarization of the cell membrane, leading to Ca2+ dependent spike discharge and development of mechanical response. Sigetin also produced deceleration of the relaxation of carbachol contracture controlled mostly by the sarcolemmal ATP driven Ca2+ pump. The drug produced strong inhibition of Mg2+, ATP-dependent Ca2+ transport in sarcolemmal vesicles as well as the enzyme and transport activity of the solubilized Ca2+, Mg(2+)-ATPase reconstructed in liposomes. Under the experimental conditions close to the physiological (i.e. in the presence of an outwardly directed Ca2+ gradient) Ca2+ pump normally compensates passive release of this cation. Sigetin was found to shift this calcium equilibrium towards a non-compensated slow diffusion of the cation in the extravesicular space. Addition of sigetin to the incubation medium during the existence of the stationary transmembrane Ca2+ equilibrium stimulates transition of the stationary concentration of the cation in vesicles from high to lower level. The results suggest that the excitatory action of sigetin on myometrial smooth muscle may involve not only indirect stimulation of Ca2+ influx via the voltage operated Ca2+ channels but also through the inhibition of the ATP driven Ca2+ pump of the cell membrane.

[Uterotonic effect of oxytocin and transport of Ca2+ through the myometrial sarcolemma]. / Uterotonicheskoe deistvie oksitotsina i transport Ca2+ cherez sarkolemmu miometriia.

Effect of oxytocin on contractile activity, passive and Mg2+, ATP-dependent Ca2+ transport through myocyte plasmic membrane was studied in the experiments carried out on intact samples of the uterus smooth muscle and fraction of myometrium sarcolemma vesicules. It was shown that at short-term (30 s) application of oxytocin (2.10(-7) M) powerful prolonged contractile reaction of myometrium bands was observed. After the chelating of Ca2+ in the washing medium by means of EGTA (2mM) or while introducing into it blockers of electrically controlled calcium channels the bands responded to oxytocin application with a single physical contraction. High concentrations of peptide hormone (10(-6) M) introduced into the preincubation medium of the smooth muscle bands before the isolation of the membrane fraction or directly into the incubation medium produced no effect on passive liberation of Ca2+ vesicules from the sarcolemma vesicules. At the same time preincubation of the bands in the solution containing smaller concentration of octapeptide (10(-7) M) decreased the initial velocity of Mg2+, ATP-dependent Ca2+ transport in the vesicules by 30% on the average. Possible mechanisms of oxytocin effects on intracellular homeostasis of Ca2+ in the myometrium, on the contractile activity of the uterus are discussed.

[The mechanism of calcium control of smooth muscle tonic contraction]. / Mekhanizm kal'tsievogo kontrolia tonicheskogo sokrashcheniia gladkoi myshtsy.

It has been shown in the experiments carried out on a fraction of inverted vesicles of myometrium sarcolemma that ATP-dependent Ca2+ transport system prevents dissipation of the calcium gradient directed from the intervesicular space outward with subsequent establishment of the stationary level of cation content inside the membrane vesicles (a blocker of electro-controlled calcium channels diltiasems was present in the incubation medium). Ortovanadatean inhibitor of the sarcolemma calcium pump suppressed Ca2+ stationary exchange in the vesicles fraction. The value of calcium stationary content in the vesicle membrane was regulated both by a change of the calcium pump activity (by varying Mg2+ concentration in the ATP-containing incubation medium), and by modification of calcium permeability of the vesicles (by varying concentration of ionophore A-23187 in this medium). In the presence of diltiasem and ortovanadate the Ca2+ basal current entering the myocytes from hyperpotassium washing solution activated the smooth muscle tonic contraction. In the absence of ortovanadate no contractile response was observed. On the basis of the evidence obtained a mechanism of calcium control of myometrium tonic contraction is proposed. According to this mechanism the Ca2+ current entering the unexcited myocytes under physiological conditions is efficiently compensated by the calcium pump of the sarcolemma. The inhibition of the latter (or an increase of the sarcolemma basal calcium permeability) provides further slow transition of the stationary value of Ca2+ concentration in the myoplasm to a new higher level and activation of the smooth muscle contraction accordingly.

[Passive Ca2+ transport in a suspension of isolated smooth-muscle cells and the contribution of the basal calcium permeability of the plasma membrane to the activation of a tonic contraction]. / Passivnyi transport Ca2+ v suspenzii izolirovannykh gladkomyshechnykh kletok i vklad bazal'noi kal'tsievoi pronitsaemosti plazmaticheskoi membrany v aktivatsiiu tonicheskogo sokrashcheniia.

Ca2+ concentration has been estimated in isolated myometrium cells using Ca2(+)-sensitive quin-2 fluorescent probe. Two components of Ca permeability of the plasmatic membrane have been determined, a potential-independent one (activated by K+ depolarization and nitrendipine-sensitive), and a basal one (not sensitive to nitrendipine). Smooth muscle cells could maintain intracellular Ca2+ concentration at the physiological level. In the presence of nitrendipine, orthovanadate, an inhibitor of sarcolemma Ca pump, induced the increase in the basal tonus depending on the presence of the Ca2+ in the medium. This suggests that in conditions of the blockage of electrically controlled Ca channels and Ca pump of the plasmatic membrane, the noncompensated basal Ca2+ influx activates the tonic contraction of smooth muscles.

[Kinetic analysis of contraction-relaxation process in smooth muscles]. / Kineticheskii analiz protsessa sokrashcheniia-rasslableniia gladkikh myshts.

A method is proposed for analysing kinetic curves of the smooth muscle contraction--relaxation approved on smooth muscle preparations of ureter and taenia coli. A notion of the velocity coefficient is introduced. It is the parameter which gives a quantitative characteristics of changes in the dynamics of muscle contraction and relaxation under the effect of factors modifying the contractile response. In order to illustrate the application of this parameter studies were carried out of the effect of sodium-free medium, monensin, and of temperature decrease on the contractile activity of the smooth muscle tissue of the ureter. The method can be useful while investigating the regularities of electro- and pharmacomechanical conjunction in the smooth muscles, as well as during pharmacological screening of compounds--regulators of calcium homeostasis in myocytes and their contractile activity.

[The role of sarcolemma calcium pump in regulating tonic smooth muscle contraction]. / Rol' kal'tsievogo nasosa sarkolemmy v reguliatsii tonicheskogo sokrashcheniia gladkoi myshtsy.

Vanadate (10(-4)-10(-3) M) effectively blocks Mg2+, ATP-dependent Ca2+ transport in sarcolemmal vesicles and induces a slowly tonic contraction of the smooth muscle. This contraction was observed both with and without nifedipine (10(-5) M) evoking complete inhibition of hyperpotassium contracture, the Ca2+ removal from the solution washing the muscular preparation stimulating the tone decrease. There is a close correlation between the dose-dependent effects of vanadate on the Ca pump activity and tension. It is concluded that in smooth muscles, at least in myometrium, the sarcolemmal Ca-pump is involved into the control of the tonic tension.

[Action of the leukotriene LTC4 on the calcium channels of the somatic membrane of the nerve cell and tone of smooth muscle organs]. / Deistvie leikotriena LTC4 na kal'tsievye kanaly somaticheskoi membrany nervnoi kletki i tonus gladkomyshechnykh organov.

Effects of synthetic leukotriene LTC4 on the internally perfused voltage-clamped snail neurons as well as on the electrical and mechanical activities of the stomach smooth muscle cells were studied. It was found that LTC4 increased calcium inward current in the soma membrane of a cell by activation of both voltage and receptor operated Ca-channels. LTC4 was effective only from outside but not from inside of the membrane which indicated that there was a receptor for leukotrienes in the neuronal membrane.

[Effect of the lipoxygenase blockader BW755C on calcium currents in the nerve cell membrane of the snail and on the contractile responses of the ureteral smooth-muscle fibers in the guinea pig]. / Vliianie blokatora lipooksigenazy BW755C na kal'tsievye toki v membrane nervnoi kletki ulitki i sokratitel'nye otvety gladkomyshechnykh volokon mochetochnika morskoi svinki.

Lipoxygenase blocker BW755C has been studied for its effect on calcium inward current in intracellularly perfused voltage clamped and contraction of guinea-pig ureter smooth muscle. BW755C increased the Ca inward current in somatic membrane and inhibited contraction of the smooth muscle evoked by high-potassium solution. It is suggested that the effects observed are related to the changes in the level of cyclic nucleotides in cytoplasm due to the action of the final products of lypoxygenase breakdown of fatty acids from the cell membrane.