Kirk P. Conrad, M.D.

Professor

Kirk P. Conrad, M.D.

Kirk P. Conrad, M.D.

(352) 392-2798
Office: MSB MG-40A
kpconrad@ufl.edu
PubMed Listing
Biosketch

Co-Director of the Reproductive and Perinatal Biology Research Program (http://www.perinatal.ufl.edu)

Research Interests

Mechanisms underlying vasodilation and increased arterial compliance during normal pregnancy with emphasis on the hormone relaxin, the RXFP1 relaxin receptor, vascular endothelial and placental growth factors, vascular MMP-2 and -9, endothelin1-32, the endothelial ETB receptor and NO (NIH R01 DK063321; NIH R01 HL067937; NIH R21 HL093605; Grant-in-Aid 0855090E; AHA Postdoctoral Fellowship to JT McGuane)

  • Relaxin and bone marrow derived progenitor cells (with Mark S. Segal, MD)
  • Potential therapeutic role of relaxin in preeclampsia (Preeclampsia Vision Award with JT McGuane from the Preeclampsia Foundation; AHA Postdoctoral Fellowship to JT McGuane)
  • Maternal cardiovascular adaptations to pregnancy in women conceiving by assisted reproductive technologies, as well as their obstetrical and neonatal outcomes (UF and UF COM Bridge Funds and NICHD P01 Resubmission (14 or 2.0%) with Mark S. Segal, MD, R. Stan Williams, MD, Maureen Keller-Wood, PhD; Keith Muller, PhD; and Valerie L. Baker, MD, Stanford).
  • Local relaxin ligand-receptor expression and function in arteries of males and females, and the consequences for cardiovascular homeostasis in vivo and as a function of aging (NIH R01 HL067937)
  • Decidualization, placentation and placental trophoblast cells, and their involvement in the etiology and pathogenesis of preeclampsia and intrauterine growth restriction (IUGR) (UF and IFAS Seed Monies), and a related interest in potential early biomarkers for preeclampsia and IUGR

In summary, one overall goal of Dr. Conrad has been to advance understanding of the mechanisms underlying maternal renal and cardiovascular adaptations to normal pregnancy. Another is to harness the “lessons learned from normal pregnancy” to facilitate the investigation of preeclampsia in which maternal vasoconstriction and arterial stiffness, as well as impaired invasion and accelerated apoptosis of trophoblast pertain. A final aim is to see the fruits of this fundamental research through to the “bedside”. Thus, consultation and collaboration on investigations of relaxin as a potential therapeutic modality in preeclampsia, as well as in various cardiovascular diseases such as acute heart failure in the non-pregnant population is another major objective.

Recent Publications:

Rajakumar A., Michael M.M., Daftary A., Jeyabalan A., Gilmour A. and Conrad K.P. Proteasomal Activity in Placentas from Women with Preeclampsia and Intrauterine Growth Restriction: Implications for Expression of HIF-alpha Proteins. Placenta 29: 290-9, 2008.

Teichman S.L., Unemori E., Dschietzig T., Conrad, K., Voors A.A., Teerlink J.R., Felker M.G., Metra M., and Cotter G.  Relaxin, a pleiotrophic vasodilator for the treatment of heart failure. Heart Failure Rev. DOI 10.1007/s10741-008-9129-3. 20 December 2008.

Founds S.A., Conley Y.P., Lyons-Weiler J.F., Jeyabalan A., Hogge W.A. and Conrad K.P. Altered global gene expression in first trimester placentas of women destined to develop preeclampsia. Placenta 30: 15-24, 2009.

Conrad K.P., Gaber L.W., and Lindheimer M.D. The Kidney in Normal Pregnancy and Preeclampsia. In:  Chesley’s Hypertensive Disorders in Pregnancy:  Third Edition. Lindheimer, M.D., Cunningham, F.G. and Roberts, J.M. (eds.).  Elsevier. 2009.

McGuane J.T., Debrah J.E., Debrah D.O., Rubin J.P., Segal M.S., Shroff S.G., and Conrad K. P. The role of relaxin in maternal systemic and renal vascular adaptations during gestation. Ann. N. Y. Acad. Sci. 1160:304-12, 2009.

Founds S. A., Terhorst L. A., Conrad K. P., Hogge W. A., Jeyabalan A. and Conley Y. P. Gene expression of eight candidates in first trimester preeclampsia placenta. Biological Research for Nursing, 2010.

Jeyabalan A., and Conrad KP. Renal Physiology and Pathophysiology in Pregnancy. In: Renal and Electrolyte Disorders. 7th edition. RW Schrier, ed. Lippincott Williams & Wilkins, Chapter 13, p. 462-518, 2010.

Conrad KP. Unveiling the vasodilatory actions and mechanisms of relaxin.  Hypertension 56:2-9, 2010 (invited review).

Conrad KP. Emerging role of relaxin in the maternal adaptations to normal pregnancy: Implications for preeclampsia.  Seminars Nephrol. 31: 15-32. 2011 (invited review).

Karamanchi A.S. and Conrad K.P. Renal Physiology and Disease in Pregnancy. In: Seldin and Giebisch’s The Kidney. Physiology and Pathophysiology: Fifth Edition. Robert J. Alpern and Steven C. Hebert, editors., in press.

McGuane J.T., Debrah J.E., Sautina L., Rubin J.P., Novak J., Segal M.S. and Conrad K.P. Relaxin induces rapid dilation of rodent small renal and human subcutaneous arteries via PI3 kinase and nitric oxide.  Endocrinol., in press.

McGuane J.T., Danielson L.A., Debrah J.E., Rubin J.P., Novak J. and Conrad K.P. Angiogenic growth factors are new players in the sustained relaxin vasodilatory pathway in rodents and humans. Hypertension, in press.

Debrah D.O., Debrah J.E., Sacks M.S., †Conrad .P. and Shroff S.G. Relaxin regulates vascular wall mechanical properties and remodeling in mice. J Appl Physiol., revised version submitted.

Conrad KP. 2010 Ernest H. Starling Lectureship. Maternal vasodilation in pregnancy: the emerging role of relaxin. Am J Physiol. Regulatory Integrative Comp. Physiol., in revision (invited review).

Recent Honors

2010 – Ernest H. Starling Distinguished Lectureship of the American Physiological Society Water & Electrolyte Homeostasis Section

2010 – Liley Lecturer Perinatal Reseach Society

2010 – Senior Faculty Research Award University of Florida Chapter Sigma XI