The calcium sensing receptor (CaR) is an understudied component of the group of mechanisms that control circulating calcium levels and are therefore intimately involved in calcium metabolism and homeostasis. Our hypothesis is that the CaR has a role in controlling calcium concentrations and fluctuations in cardiac dysfunction, and might be a compensatory mechanism due to the loss of the more traditional mechanisms of calcium transport in the excitation-contraction pathway. As a model for acute stress, we will employ a burn model that is currently used at UTMB-Galveston to study mechanisms of post-burn bone loss and the involvement of the parathormone-calcitonin pathway. This model has yielded data regarding down-regulation of parathyroid CaR and leads to acute cardiac distress.

Our goal is to understand the role of the CaR in cardiac dysfunction and heart failure associated with severe, acute trauma. Initially we will use the acute stress tissue from the ovine source. We then plan to expand our experimentation as an extension of our studies of mechanisms associated with heart failure and recovery, and examine the involvement of the CaR in chronic heart disease, intestinal dysfunction and burns.

Collaborators:

  • Dr. Gordon Klein, UTMB-Galveston
  • Dr. O. H. Frazier, Texas Heart Institute