Viveka Gajendiran

National University of Singapore, Singapore, Singapore

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Publications (4)2.15 Total impact

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    ABSTRACT: Gastrointestinal (GI) motility is coordinated by several cooperating mechanisms, including electrical slow wave activity, the enteric nervous system (ENS), and other factors. Slow waves generated in interstitial cells of Cajal (ICC) depolarize smooth muscle cells (SMC), generating basic GI contractions. This unique electrical coupling presents an added layer of complexity to GI electromechanical models, and a current barrier to further progress is the lack of a framework for ICC-SMC-contraction coupling. In this study, an initial framework for the electromechanical coupling was developed in a 2-D model. At each solution step, the slow wave propagation was solved first and [Ca(2+)](i) in the SMC model was related to a Ca(2+)-tension-extension relationship to simulate active contraction. With identification of more GI-specific constitutive laws and material parameters, the ICC-SMC-contraction approach may underpin future GI electromechanical models of health and disease states.
    IEEE transactions on bio-medical engineering 08/2011; 58(12):3491-5. · 2.15 Impact Factor
  • IEEE Trans. Biomed. Engineering. 01/2011; 58:3491-3495.
  • Viveka Gajendiran, Martin L. Buist
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    ABSTRACT: A mathematical model to describe the relationship between the intracellular Ca2+ concentration and active force production in a gastrointestinal (GI) smooth muscle cell (SMC) has been developed. Here the model has been constructed in terms of two modules, the first describing the activation of myosin light chain kinase (MLCK) through its interactions with calmodulin and Ca2+ ions, and the second consisting of a four state scheme describing myosin phosphorylation and cross-bridge formation between actin and myosin. A prescribed Ca2+ transient, representing the dynamic changes in intracellular free Ca2+ that accompanies GI SMC excitation, was used as the input signal. Simulations demonstrated that at physiological Ca2+ levels, a 33% increase in peak Ca2+ concentration resulted in a 93% increase in myosin phosphorylation. This can possibly be attributed to the steep relationship between Ca2+ and MLCK activation over the normal Ca2+ range. The total number of cross-bridges (sum of cycling cross-bridges and latch-bridges) was used to predict the active force generated in response to a phasic Ca2+ signal. The predicted forces were in qualitative agreement with experimental data from a canine antral smooth muscle strip. The development of this model represents a first step towards a greater understanding of the mechanisms that underlie GI motility. Copyright © 2010 John Wiley & Sons, Ltd.
    International Journal for Numerical Methods in Biomedical Engineering. 11/2010; 27(3):450 - 460.
  • Viveka Gajendiran, Martin L. Buist
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    ABSTRACT: In the gastrointestinal (GI) system, motility is governed by the contraction and relaxation of smooth muscle (SM) in response to many regulatory factors. SM in a hollow organ like stomach exhibits two types of contraction: tonic, to maintain the shape of the organ, and phasic, in response to neurotransmitters, hormones or other signaling molecules. Motility disorders such as dysphagia, gastroesophageal reflux disease, irritable bowel syndrome and hypotensive or hypertensive disorders all involve abnormal SM function. Hence, it is important to gain a deeper understanding of contraction and its regulation in GI SM cells. Skeletal muscle cells have force-velocity curves in which shortening velocities are determined only by load and the myosin isoform. In contrast, when smooth muscle activation is altered, e.g. by changing a hormone or agonist concentration, a different set of velocity-stress curves can be obtained. This difference is due to the regulation of both the number of active cross bridges (determining force) and their average cycling rates (determining the velocity). The regulatory system depends on the phosphorylation of cross-bridges, which in turn depends on cytosolic Ca2+ levels. Thus, a model has been proposed to study the effects of (a) Ca2+ concentration on the kinetics of myosin phosphorylation, (b) cross-bridge cycling rates, and (c) the latch state on tonic and phasic contractions. The objective of the model is to describe the regulation of myosin phosphorylation and active stress production in terms of the intracellular Ca2+ concentration. A mathematical formulation of cross bridge cycling has been adapted from the literature and the parameters have been fitted to experimental data from GI SM. Here it was assumed that the Ca2+-calmodulin mediated phosphorylation of myosin is the primary determinant of the kinetics of cross bridge cycling. This model is the first step towards developing a dynamic model of GI SM contraction.

Publication Stats

4 Citations
2.15 Total Impact Points


  • 2010
    • National University of Singapore
      • Department of Bioengineering
      Singapore, Singapore