Kirk P. Conrad, M.D.

J. Robert and Mary Cade Professor of PhysiologyConrad, Kirk

Phone: (352) 392-2798
Office: MSB MG-40A

Education and Training/Previous Appointments

  • 2014-17: Grant Awards Committee, Society for Reproductive Investigation
  • 2010-14: Secretary Treasurer: Society for Gynecological Investigation
  • 2007-10: Council Member: Society for Gynecological Investigation
  • 2004: Sabbatical: Honorary Fellow Department of Zoology, University of Melbourne, Parkville, Victoria, Australia
  • 1996-2006: Tenure Status: Department of Ob/Gyn and Reproductive Sciences, University of Pittsburgh School of Medicine, Pittsburgh, PA
  • 2000-2006: Professor (Primary Appointment) Department of Ob/Gyn and Reproductive Sciences, and Professor (Secondary Appointment) Department of Cell Biology and Physiology: University of Pittsburgh School of Medicine, Pittsburgh, PA
  • 2000-03 Member: NIH Human Embryology and Development Study Section-1
  • 1994-99: Associate Professor: Department of Ob/Gyn and Reproductive Sciences, University of Pittsburgh School of Medicine, Pittsburgh, PA
  • 1996-99: Associate Professor (Secondary Appointment): Department of Cell Biology and Physiology, University of Pittsburgh School of Medicine, Pittsburgh, PA
  • 1992-94: Associate Professor: Departments of Physiology and of Ob/Gyn, University of New Mexico School of Medicine, Albuquerque, NM
  • 1990-92: Assistant Professor: Departments of Physiology and of Ob/Gyn, University of New Mexico School of Medicine, Albuquerque, NM
  • 1984-90: Assistant Professor: Department of Physiology, Dartmouth Medical School, Hanover, NH
  • 1985-87: Visiting Instructor/Postdoctoral Fellow: Case Western Reserve University, Cleveland, OH (Renal/Cell Physiology)
  • 1981-84: Postdoctoral Fellow: Dartmouth Medical School, Hanover, NH (Renal Physiology)
  • 1980-81: Medical Intern: University of Colorado Health Sciences Center, Denver, CO (Medicine)
  • 1980: M.D.: Dartmouth Medical School, Hanover, NH (Medicine)
  • 1977: B.A.: Bowdoin College, Brunswick, ME (Biochemistry)

Research Interests

A long-standing research interest is to understand the mechanisms underlying the massive systemic maternal vasodilation and increased arterial compliance that transpire during normal pregnancy. Another is the dysregulation of these maternal circulatory adaptations in preeclampsia (a hypertensive disease of pregnancy), and the potential etiological role of aberrant endometrial maturation in the defective placentation associated with preeclampsia and other placental syndromes such as intrauterine growth restriction. Ultimately the goal is to apply the new knowledge gained from these investigations towards the development of mechanistic-based preventative, therapeutic and curative measures for these obstetrical diseases.

We found that the ovarian hormone relaxin is a potent vasodilator in the systemic and renal circulations, and that it contributes to the remarkable changes in the vasculature during pregnancy. These discoveries provided scientific basis and motivation for pursuing the hormone as a therapy for afterload reduction and improvement of renal function in heart failure ( Identifier: CRLX030A2301), and they further suggested a therapeutic role in preeclampsia. We unveiled endothelial mechanisms of systemic vasodilation in pregnancy, and then our independent investigations of the cardiovascular effects of pregnancy and relaxin converged, leading to the elucidation of endothelial mechanisms for both “rapid” and “sustained” vasodilation by relaxin. We also observed that, unexpectedly, relaxin was equally potent in the vasculature of males, and to explain this finding we hypothesized the existence of local relaxin ligand-receptor expression and function in arteries, which we subsequently supported with both molecular and functional evidence. More recently, we found a new role for relaxin in bone marrow angiogenic progenitor cell mobilization and function, and in the context of pregnancy. A final aim has been to apply the “lessons learned from pregnancy” to further understand and treat cardiovascular disease in the non-pregnant population (e.g., heart failure).

We always strive to translate discoveries made in preclinical investigations to humans. As one example, we are currently investigating the cardiovascular adaptations and obstetrical outcomes of pregnancies in women conceiving by Assisted Reproductive Technologies (ART) (in comparison to spontaneously conceived pregnancies), because ART occurs in the setting of nil or as many as 20 corpora lutea, thus dramatically effecting the circulating levels of relaxin and other potentially vasoactive corpus luteal hormones. As another example, we investigated global gene expression in chorionic villus samples from women who later developed preeclampsia. After secondary analyses of the 356 genes altered in the CVS from women who developed preeclampsia, we find that as many as 154 genes are associated with decidualization or in this case, inadequate decidualization. Dr. Conrad and colleagues at the University of Florida are well situated to take these exciting findings to the next level. A long-term goal is to understand the etiology of preeclampsia, which will facilitate discovery of biomarkers for disease prediction, and strategies for prophylaxis and therapy. We believe that it is especially important to integrate Reproductive and Perinatal Medicine, in order to unveil etiology and develop preventative therapies for adverse pregnancy and neonatal outcomes.


Organizer of the Reproductive and Perinatal Biology Research Program (2008-2018) (

Teaching (Including Courses)

  • Principles of Physiology (GMS 6400C)
  • Fundamentals of Endocrine Physiology (GMS 6405)
  • Advanced Topics in Hypertension Research (GMS 6413)
  • Advanced Renal Physiology (GMS 6414)
  • Medical Endocrine and Reproductive Physiology (GMS 6419)
  • Human Physiology for Physician Assistants (PAS 5025)
  • Dental Physiology (DEN 5120C)
  • Endocrinology and Reproduction (BMS 6632)
  • Kidney and Urinary Tract (BMS 6638C)

Awards and Honors

  • 2019: Interviewed by the American Heart Association for their article titled, “Why Do IVF Pregnancies With Frozen Embryos Raise Preeclamsia Risk?
  • 2018-21: University Term Professorship award from the University of Florida in recognition of academic accomplishment.
  • 2013, 2014, 2016: Exemplary Teacher Award, University of Florida College of Medicine
  • 2012: Dutch Heart Foundation Lecturer
  • 2010: Ernest H. Starling Distinguished Lectureship of the American Physiological Society Water & Electrolyte Homeostasis Section
  • 2010: Liley Lecturer Perinatal Research Society
  • 2010: Senior Faculty Research Award University of Florida Chapter Sigma XI
  • 1995-99: Research Career Development Award (KO4 HD01098)
  • 1993: Basic Medical Sciences Teaching Award presented by UNM Sch. of Medicine Graduates
  • 1991-94: Flinn Newly Independent Investigator Award (American Heart Association)
  • 1990: Outstanding Teacher Award in the Basic Sciences
  • 1988-1993: 8th Mallinckrodt Scholar Award
  • 1985-1990: Physician Scientist Award (K11 HD00662)
  • 1980: Good Physicians Award (Dartmouth Medical School)
  • 1979: Alpha Omega Alpha Honor Society
  • 1976: James Bowdon Honor Society
Conrad Lab, 2017
Conrad Lab, 2017


PubMed Listing

*Recent Representative Publications Listed Below*
  • Taher, S., Borja, Y., Cabanela, L., Costers, V. J., Carson-Marino, M., Bailes, J. C., Dhar, B., Beckworth, M. T., Rabaglino, M. B., Post Uiterweer, E. D., … Conrad, K. P. (2019). Cholecystokinin, Gastrin, Cholecystokinin/Gastrin Receptors, and Bitter Taste Receptor, TAS2R14: Trophoblast Expression and Signaling. American journal of physiology. Regulatory, integrative and comparative physiology, in press. (PMID: 30892908)
  • von Versen-Höynck, F., Narasimhan, P., Selamet Tierney, E. S., Martinez, N., Conrad, K. P., Baker, V. L., … Winn, V. D. (2019). Absent or Excessive Corpus Luteum Number is Associated with Altered Maternal Vascular Health in Early Pregnancy. Hypertension, 73(3), 680-690. (PMID: 30636549; PMCID: PMC6378337)
  • von Versen-Höynck, F., Schaub, A. M., Chi, Y. Y., Chiu, K. H., Liu, J., Lingis, M., Williams, R. S., Rhoton-Vlasak, A., Nichols, W. W., Fleischmann, R. R., Zhang, W., Winn, V. D., Segal, M. S., Conrad K. P., … Baker V. L. (2019). Increased preeclampsia risk and reduced aortic compliance with in vitro fertilization cycles in the absence of a corpus luteum. Hypertension, 73(3), 640-649. (PMID: 30636552)
  • Deng, A., Conrad, K., & Baylis, C. (2018). Relaxin mediated renal vasodilation in the rat is associated with falls in glomerular blood pressure. American journal of physiology. Regulatory, integrative and comparative physiology, 314(2), R147-R152. doi: 10.1152/ajpregu.00148.2017. (PMID: 29046312; PMCID: PMC5867670)
  • Conrad K. P., Rabaglino M.B., & Post Uiterweer E.D. (2017). Emerging role for dysregulated decidualization in the genesis of preeclampsia. Placenta, 60, 119-129. doi: 10.1016/j.placenta.2017.06.005. (PMID: 28693893; PMCID: PMC5718949)
  • Ogunleye, O., Campo, B., Herrera, D., Post Uiterweer, E. D., & Conrad, K. P. (2017). Relaxin confers cytotrophoblast protection from hypoxia-reoxygenation injury through the phosphatidylinositol 3-kinase-Akt/protein kinase B cell survival pathway. American journal of physiology. Regulatory, integrative and comparative physiology, 312(4), R559-R568. (PMID: 28122716; PMCID: PMC5407077)
  • Leo, C. H., Jelinic, M., Ng, H. H., Marshall, S. A., Novak, J., Tare, M., Conrad, K. P., … Parry, L. J. (2016). Vascular actions of relaxin: nitric oxide and beyond. British journal of pharmacology, 174(10), 1002-1014. (PMID: 27590257; PMCID: PMC5406296)
  • Conrad, K. P. (2016). G-Protein-coupled receptors as potential drug candidates in preeclampsia: targeting the relaxin/insulin-like family peptide receptor 1 for treatment and prevention. Human reproduction update, 22(5), 647-64. (PMID: 27385360; PMCID: PMC5001498)
  • Rabaglino, M. B., Post Uiterweer, E. D., Jeyabalan, A., Hogge, W. A., & Conrad, K. P. (2014). Bioinformatics approach reveals evidence for impaired endometrial maturation before and during early pregnancy in women who developed preeclampsia. Hypertension (Dallas, Tex. : 1979)65(2), 421-9. (PMID: 25421975; PMCID: PMC4290371)
  • Conrad, K. P., & Davison, J. M. (2014). The renal circulation in normal pregnancy and preeclampsia: is there a place for relaxin?. American journal of physiology. Renal physiology306(10), F1121-35. (PMID: 24647709; PMCID: PMC4024736)

For additional publications and current grant support, see CV.