TRAINING PROGRAM IN CARDIOVASCULAR PHARMACOLOGY

Summary

Principal Investigator: Joey Barnett
Abstract: The integration of our scientific knowledge of cardiovascular function at the molecular, cellular, and organismal levels is critical to impacting cardiovascular disease in humans. As our insight into molecular and cellular processes has grown, emphasis in many Ph.D. training programs has shifted away from integrated (whole animal or systems) biology. The lack of an available scientific workforce with an understanding of integrated biology, including drug metabolism and pharmacokinetics, and an appreciation of the unique challenges of working in intact organisms will delay the application of discoveries at the molecular and cellular levels to human disease. This training program addresses a critical need for scientists trained in the integrated biology of the cardiovascular system. Our program uses existing strengths in the Department of Pharmacology at Vanderbilt University and key collaborators who direct well established research programs in cardiovascular pharmacology and biology. The primary activity of trainees is research training on issues related to cardiovascular function and disease under the direction of an individual faculty mentor. The usual duration of training is 2-3 years and fellows with Ph.D. and M.D. degrees will be supported. Research training is supplemented with focused didactic lectures on drug metabolism and pharmacokinetics, cardiovascular physiology, and cardiovascular pharmacology (all part of the existing core curriculum of the Predoctoral Pharmacology Training Program). Fellows will be required to participate in Responsibility in Research training and weekly seminar series in Experimental Therapeutics, Cardiovascular Medicine, and Pharmacology. Trainees may elect to participate in the Vanderbilt Master of Science in Clinical Investigation Program. Our specific goals are to provide trainees with expertise in the integrated biology of the cardiovascular system, encourage collaboration between laboratories using whole animal and molecular approaches, and develop scientists trained to participate in drug discovery and drug development in the cardiovascular system. Our overall goal is to train scientists who will be leaders in academia, industry, or regulatory affairs.
Funding Period: 2004-05-01 - 2010-04-30
more information: NIH RePORT

Top Publications

  1. pmc Transforming growth factor-beta stimulates epithelial-mesenchymal transformation in the proepicardium
    Harold E Olivey
    Department of Pharmacology, Vanderbilt University Medical Center, Nashville, Tennessee 37232 6600, USA
    Dev Dyn 235:50-9. 2006
  2. pmc Methamphetamine reduces LTP and increases baseline synaptic transmission in the CA1 region of mouse hippocampus
    Jarod Swant
    Neuroscience and Pharmacology, Meharry Medical College, Nashville, Tennessee, United States of America
    PLoS ONE 5:e11382. 2010
  3. pmc Transcriptional remodeling of rapidly stimulated HL-1 atrial myocytes exhibits concordance with human atrial fibrillation
    Lisa C Mace
    Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN 37232 6602, USA
    J Mol Cell Cardiol 47:485-92. 2009
  4. ncbi The Kir channel immunoglobulin domain is essential for Kir1.1 (ROMK) thermodynamic stability, trafficking and gating
    Katherine Fallen
    Department of Anesthesiology, Vanderbilt University Medical Center, Nashville, TN 37232, USA
    Channels (Austin) 3:57-68. 2009
  5. pmc Amphetamine and methamphetamine differentially affect dopamine transporters in vitro and in vivo
    J Shawn Goodwin
    Department of Neurobiology and Neurotoxicology and Cancer Biology, Meharry Medical College, Nashville, TN 37208, USA
    J Biol Chem 284:2978-89. 2009
  6. ncbi Primary and immortalized mouse epicardial cells undergo differentiation in response to TGFbeta
    Anita F Austin
    Department of Pharmacology, Vanderbilt University Medical Center, Nashville, Tennessee 37232 6600, USA
    Dev Dyn 237:366-76. 2008
  7. pmc Bradykinin type 2 receptor BE1 genotype influences bradykinin-dependent vasodilation during angiotensin-converting enzyme inhibition
    Gary P Van Guilder
    Division of Clinical Pharmacology, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN 37232 6602, USA
    Hypertension 51:454-9. 2008
  8. pmc Dipeptidyl peptidase IV in angiotensin-converting enzyme inhibitor associated angioedema
    James Brian Byrd
    Department of Medicine, Vanderbilt University Medical School, Nashville, TN, USA
    Hypertension 51:141-7. 2008
  9. ncbi Dipeptidyl peptidase IV deficiency increases susceptibility to angiotensin-converting enzyme inhibitor-induced peritracheal edema
    James Brian Byrd
    Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN, USA
    J Allergy Clin Immunol 120:403-8. 2007
  10. ncbi Angiotensin-converting enzyme inhibitor-associated angioedema
    James Brian Byrd
    Division of Clinical Pharmacology, Vanderbilt University School of Medicine, 560 Robinson Research Building, Nashville, TN 37232 6602, USA
    Immunol Allergy Clin North Am 26:725-37. 2006

Detail Information

Publications12

  1. pmc Transforming growth factor-beta stimulates epithelial-mesenchymal transformation in the proepicardium
    Harold E Olivey
    Department of Pharmacology, Vanderbilt University Medical Center, Nashville, Tennessee 37232 6600, USA
    Dev Dyn 235:50-9. 2006
    ..These data demonstrate that TGFbeta stimulates transformation in the PE and suggest that ALK2 partially mediates this effect...
  2. pmc Methamphetamine reduces LTP and increases baseline synaptic transmission in the CA1 region of mouse hippocampus
    Jarod Swant
    Neuroscience and Pharmacology, Meharry Medical College, Nashville, Tennessee, United States of America
    PLoS ONE 5:e11382. 2010
    ..This modulation may contribute to synaptic maladaption induced by METH addiction and/or METH-mediated cognitive dysfunction...
  3. pmc Transcriptional remodeling of rapidly stimulated HL-1 atrial myocytes exhibits concordance with human atrial fibrillation
    Lisa C Mace
    Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN 37232 6602, USA
    J Mol Cell Cardiol 47:485-92. 2009
    ..Importantly, we identified novel pathways and molecules that were concordantly regulated in vivo...
  4. ncbi The Kir channel immunoglobulin domain is essential for Kir1.1 (ROMK) thermodynamic stability, trafficking and gating
    Katherine Fallen
    Department of Anesthesiology, Vanderbilt University Medical Center, Nashville, TN 37232, USA
    Channels (Austin) 3:57-68. 2009
    ..Our study sheds new light on the pathogenesis of ABS and establishes the IgLD as an essential structure within the Kir channel family...
  5. pmc Amphetamine and methamphetamine differentially affect dopamine transporters in vitro and in vivo
    J Shawn Goodwin
    Department of Neurobiology and Neurotoxicology and Cancer Biology, Meharry Medical College, Nashville, TN 37208, USA
    J Biol Chem 284:2978-89. 2009
    ..Together these data demonstrate that METH has a stronger effect on DAT-mediated cell physiology than AMPH, which may contribute to the euphoric and addictive properties of METH compared with AMPH...
  6. ncbi Primary and immortalized mouse epicardial cells undergo differentiation in response to TGFbeta
    Anita F Austin
    Department of Pharmacology, Vanderbilt University Medical Center, Nashville, Tennessee 37232 6600, USA
    Dev Dyn 237:366-76. 2008
    ..These data demonstrate that TGFbeta induces epicardial cell differentiation and that immortalized epicardial cells provide a suitable model for differentiation...
  7. pmc Bradykinin type 2 receptor BE1 genotype influences bradykinin-dependent vasodilation during angiotensin-converting enzyme inhibition
    Gary P Van Guilder
    Division of Clinical Pharmacology, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN 37232 6602, USA
    Hypertension 51:454-9. 2008
    ..In conclusion, the BDKRB2 BE1 polymorphism influences bradykinin type 2 receptor-mediated vasodilation during angiotensin-converting enzyme inhibition...
  8. pmc Dipeptidyl peptidase IV in angiotensin-converting enzyme inhibitor associated angioedema
    James Brian Byrd
    Department of Medicine, Vanderbilt University Medical School, Nashville, TN, USA
    Hypertension 51:141-7. 2008
    ..Environmental or genetic factors that reduce dipeptidyl peptidase IV activity may predispose individuals to angioedema...
  9. ncbi Dipeptidyl peptidase IV deficiency increases susceptibility to angiotensin-converting enzyme inhibitor-induced peritracheal edema
    James Brian Byrd
    Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN, USA
    J Allergy Clin Immunol 120:403-8. 2007
    ..ACE and DPPIV degrade substance P, an edema-forming peptide. The contribution of impaired degradation of substance P by DPPIV to the pathogenesis of ACE inhibitor-associated angioedema is unknown...
  10. ncbi Angiotensin-converting enzyme inhibitor-associated angioedema
    James Brian Byrd
    Division of Clinical Pharmacology, Vanderbilt University School of Medicine, 560 Robinson Research Building, Nashville, TN 37232 6602, USA
    Immunol Allergy Clin North Am 26:725-37. 2006
    ..Defective degradation of vasoactive peptide substrates of ACE, such as bradykinin or substance P, may contribute via non-ACE pathways to the pathogenesis of ACE inhibitor-associated angioedema...
  11. pmc PAR4, but not PAR1, signals human platelet aggregation via Ca2+ mobilization and synergistic P2Y12 receptor activation
    Michael Holinstat
    Department of Pharmacology, Vanderbilt University Medical Center, Nashville, Tennessee 37232 6600, USA
    J Biol Chem 281:26665-74. 2006
    ..Thus, our data identify an intra-platelet mechanism that may function as a future site for therapeutic intervention...
  12. pmc Interactive hemodynamic effects of dipeptidyl peptidase-IV inhibition and angiotensin-converting enzyme inhibition in humans
    Annis Marney
    Division of Endocrinology, Department of Medicine, University of Vermont, Colchester, VT 05446, USA
    Hypertension 56:728-33. 2010
    ..This study provides the first evidence for an interactive hemodynamic effect of dipeptidyl peptidase-IV and ACE inhibition in humans...