Some electrical properties of human pregnant myometrium

“…Two types of VDCC, T-and L-type, have been identified in the human myometrium using electrophysiological methods [10], and may also be present in the rat myometrium [11,12]. As the T-type VDCC is thought to generate the pacemaker potential and to contribute to cell differentiation in myoblasts and neurons [13][14][15][16], examination of the expression of T-and L-type VDCC mRNAs in both muscle layers during pregnancy may provide important clues to the nature of the molecular mechanism responsible for the excitability of uterine smooth muscle cells.…”

Section: Introductionmentioning

confidence: 99%

Differential Expression of L- and T-Type Calcium Channels between Longitudinal and Circular Muscles of the Rat Myometrium during Pregnancy

Ohkubo

Kawarabayashi

Inoue

et al. 2005

Gynecol Obstet Invest

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The aim of this study was to evaluate the difference in the expression of mRNA of two types of calcium channels between longitudinal and circular muscle layer of rat myometrium during pregnancy. Changes in the expressions of the mRNA encoding L-type (α1C) and T-type (α1G, α1H, and α1I) calcium channels in longitudinal and circular smooth muscle cells of the rat myometrium were examined using a comparative kinetic RT/PCR method. During the course of pregnancy, α1C mRNA expression showed an N-shaped change in longitudinal muscle, but simply increased after mid-pregnancy in circular muscles. The mRNAs for α1G and α1H, but not that for α1I, were expressed in both longitudinal and circular smooth muscle. In longitudinal muscle, the change in α1H mRNA was similar to that in α1C mRNA during gestation, but the expression of α1G mRNA changed significantly only at term (day 22). In circular muscle, α1H mRNA expression was stable at any stage during pregnancy, but α1G mRNA significantly increased on day 15 and at term. No relationship was observed between voltage-dependent calcium-channel mRNA expressions and either proliferation or hypertrophy of circular muscle during pregnancy. These results show (a) that during pregnancy, the expression levels of L-type channels change dynamically, and it may contribute directly to the regulation of cell excitability, and (b) that the T-subtype that increases during pregnancy differs between longitudinal and circular muscle cells, although their functions remain unclear.

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“…[7][8][9]. Stress production by the contracting cell is described using the four-state cross-bridge model of Hai and Murphy (5), which was developed for arterial and tracheal SMCs.…”

Section: Description Of the Modelmentioning

confidence: 99%

“…Stimulation of isolated myocytes using voltage pulses revealed the current-voltage relationships of the pregnant myometrial SMCs in rats (18,34) and in humans (7,37). Application of single voltage pulses demonstrated that the Ca 2ϩ current (I Ca ) through L-type VOCCs significantly increased C Ca,i , whereas repetitive stimulation with pulse trains revealed that both VOCC opening and Ca 2ϩ -induced Ca 2ϩ release (CICR) from the sarcoplasmic reticulum (SR) are responsible for the increased C Ca,i (18).…”

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confidence: 99%

“…The predicted variations in C Ca,i , MLC phosphorylation, and stress produced by the contracting myocytes are compared with experimental data from human and rat myometrial cells. Rate constant of phosphorylation of AM to AM p (1/s) K 2 Rate constant of dephosphorylation of M p to M (1/s) K 5 Rate constant of dephosphorylation of AM p to AM (1/s) K 3 Rate constant of attachment of fast cycling phosphorylated cross bridges (1/s) K 4 Rate constant of detachment of fast cycling phosphorylated cross bridges (1/s) K 7 Rate constant of latch bridge detachment (1/s) …”

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Mathematical model of excitation-contraction in a uterine smooth muscle cell

Bursztyn¹,

Eytan²,

Jaffa³

et al. 2007

American Journal of Physiology-Cell Physiology

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Uterine contractility is generated by contractions of myometrial smooth muscle cells (SMCs) that compose most of the myometrial layer of the uterine wall. Calcium ion (Ca 2ϩ ) entry into the cell can be initiated by depolarization of the cell membrane. The increase in the free Ca 2ϩ concentration within the cell initiates a chain of reactions, which lead to formation of cross bridges between actin and myosin filaments, and thereby the cell contracts. During contraction the SMC shortens while it exerts forces on neighboring cells. A mathematical model of myometrial SMC contraction has been developed to study this process of excitation and contraction. The model can be used to describe the intracellular Ca 2ϩ concentration and stress produced by the cell in response to depolarization of the cell membrane. The model accounts for the operation of three Ca 2ϩ control mechanisms: voltage-operated Ca 2ϩ channels, Ca 2ϩ pumps, and Na ϩ /Ca 2ϩ exchangers. The processes of myosin light chain (MLC) phosphorylation and stress production are accounted for using the cross-bridge model of Hai and Murphy (Am J Physiol Cell Physiol 254: C99 -C106, 1988) and are coupled to the Ca 2ϩ concentration through the rate constant of myosin phosphorylation. Measurements of Ca 2ϩ , MLC phosphorylation, and force in contracting cells were used to set the model parameters and test its ability to predict the cell response to stimulation. The model has been used to reproduce results of voltage-clamp experiments performed in myometrial cells of pregnant rats as well as the results of simultaneous measurements of MLC phosphorylation and force production in human nonpregnant myometrial cells. cellular calcium control mechanisms; myometrial contractions; myosin light chain phosphorylation UTERINE CONTRACTILITY is generated by contractions of the myometrial smooth muscle cells (SMCs) that compose most of the myometrial layer of the uterine wall. In the nonpregnant uterus, synchronous contractions of these SMCs produce changes in the geometry of the uterine fluid-wall interface. These changes induce intrauterine fluid motions that are essential during early phases of reproduction (3,11,28). During parturition, the synchronized contraction of these myocytes generates the forces required to deliver the baby out of the uterus. Depolarization of the cell membrane initiates calcium ion (Ca 2ϩ ) entry into the cells through voltage-operated Ca 2ϩ channels (VOCCs) and thereby a rise in the intracellular Ca 2ϩ concentration (C Ca,i ). The elevated level of C Ca,i allows binding of Ca 2ϩ and calmodulin, thus activating myosin light-chain kinase (MLCK), which phosphorylates a regulatory myosin light chain (MLC) (29,32). This subsequently allows the formation of cross bridges between actin and myosin filaments and the generation of muscle contraction.The excitation-contraction process was studied in both rat and human myometria using the voltage-clamp technique. Stimulation of isolated myocytes using voltage pulses revealed the current-voltage relationship...

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Some electrical properties of human pregnant myometrium

Cited by 69 publications

References 12 publications

T-type Ca2+ channels in non-vascular smooth muscles

T-type Ca2+ channels in non-vascular smooth muscles

Differential Expression of L- and T-Type Calcium Channels between Longitudinal and Circular Muscles of the Rat Myometrium during Pregnancy

Mathematical model of excitation-contraction in a uterine smooth muscle cell

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