Kirk P. Conrad, M.D.
Professor
Departments of Physiology and Functional Genomics,
and of Obstetrics and Gynecology
University of Florida College of Medicine
1600 SW Archer Rd., M552
PO Box 100274
Gainesville, FL 32610
Phone: (352) 392-2798 Fax: (352) 846-0270
Office: MG40A
E-mail: kpconrad@ufl.edu
Publications: Search PubMed
Education and Training
Bowdoin College, Brunswick, ME
Dartmouth Medical School, Hanover, NH
Univ of Colorado Health Sciences Ctr, Denver, CO
DEGREE
(if applicable)
BA
MD
Medical Intern
Dartmouth Medical School, Hanover, NH
Postdoc
1981-1984
Case Western Reserve University, Cleveland, OH
Visiting Instructor/
Postdoc
1985-1987
INSTITUTION AND LOCATION
YEAR(s)
1977
1980
1980-1981
FIELD
OF
STUDY
Biochemistry
Medicine
Medicine
Renal
Physiology
Cell Physiology
Research Interests and Funding Sources
Dr. Conrad’s major research interests cover three general areas involving both fundamental and clinical research. (1)
Investigation of the mechanisms underlying the remarkable renal and systemic vasodilation and increased arterial
compliance during normal pregnancy. Dr. Conrad and colleagues identified the ovarian hormone, relaxin, as a major
hormonal signal. They further elucidated the cellular signaling pathway by which relaxin mediates vasodilation: angiogenic
growth factors, vascular gelatinases, the endothelial endothelin B receptor and nitric oxide. Further dissection of the
cellular and molecular mechanisms of vasodilation and alterations of arterial compliance by relaxin are ongoing (NIH RO1
DK63321-15, NIH HL67937-06 and AHA Grant in Aid). Preclinical evaluation of relaxin efficacy in an animal model of
preeclampsia has won funding from the Preeclampsia Foundation with additional NIH funds pending. Further clinical
investigation of the role of relaxin in maternal adaptations to human pregnancy is being planned in patients conceiving by
assisted reproductive technologies (ART). (2) Dr. Conrad and coworkers recently discovered that there is a relaxin
hormone/relaxin receptor system locally expressed by arteries in the nonpregnant condition irrespective of gender which
potently regulates arterial behavior—both myogenic reactivity and passive compliance. Investigation of the impact of this
vascular relaxin system in conscious, chronically instrumented mice and as a function of aging is currently in progress
(NIH RO1 HL67937-06). (3) The third area of research deals with abnormal placentation and cardiovascular
maladaptation in preeclampsia. Dr. Conrad and colleagues have focused on the hypoxia inducible transcription factors in
the human placenta and their role in the etiology and pathogenesis of preeclampsia (recently Subproject #2 of PO1
HD30367 and funding in transition). In addition, they have recently completed a microarray analysis of first trimester
placentas from women destined to develop preeclampsia that provides early clues to etiology and biomarkers of disease.
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 abnormal vasoconstriction and arterial stiffness pertain.
A final aim is to see the fruits of this research through to the “bedside”. Thus, consultation and collaboration on
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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 (and ones currently underway).
Recent Publications
Original works
Rajakumar A., Doty K.D., Daftary A., Markovic N., and Conrad K.P. Expression of von Hippel Lindau protein in placentae
from women with normal pregnancy and preeclampsia. Placenta 27:411-421. 2006.
Smith M.C., Murdoch A.P., Danielson L.A., Conrad K.P. and Davison J.M. Relaxin has a role in establishing a renal
response in pregnancy. Fertility and Sterility 86:253-255, 2006.
Jeyabalan A., Kerchner L.J., Fisher M.C., McGuane J.T., Doty K.D., and Conrad K.P. Matrix metalloproteinase-2 activity,
protein, mRNA and tissue inhibitors in small arteries from pregnant and relaxin-treated nonpregnant rats. J Applied
Physiol. 100:1955-1963, 2006.
Smith M.C., Danielson L.A., Conrad K.P., and Davison J.M. Influence of recombinant human relaxin on renal
haemodynamics in humans. J Am Soc Nephrol. 17:3192-7, 2006.
Novak J., Parry L.J., Matthews J., Kerchner L.J., Indovina K., Hanley-Yanez K., Doty K.D., Debrah D.O., Shroff S.G., and
Conrad K.P. Identification of relaxin ligand-receptor expression and function in arteries. FASEB J. 20:2352-62, 2006.
Debrah D.O., Novak J., Matthews J.E., Ramirez R.J., Shroff S.G., and Conrad K.P. Relaxin is essential for systemic
vasodilation and increased global arterial compliance during early pregnancy in conscious rats. Endocrinol. 147:5126-31,
2006.
Jeyabalan A., Novak J., Doty K.D., Matthews J., Fisher M.C., Kerchner L.J., and Conrad K.P. Vascular matrix
metalloproteinase-9 mediates the inhibition of myogenic reactivity in small arteries isolated from rats after short term
administration of relaxin. Endocrinol., 148:189-97, 2007.
Rajakumar A., Jeyabalan A., Markovic N., Ness R., Gilmore C., and Conrad K.P. Placental HIF-1α, HIF-2α, membrane
and soluble VEGF receptor-1 proteins are not increased in normotensive pregnancies complicated by late onset
intrauterine growth restriction. Am. J. Physiol. Regulatory Integrative Comp. Physiol. 293:R766-74, 2007.
.
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.
Founds S.F., 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 Revised version
submitted.
Book Chapters and Invited Reviews
Jeyabalan A. and Conrad K.P. Renal Function during Normal Pregnancy and Preeclampsia. Front Biosci. 12:2425-37,
2007.
Lindheimer M.D., Conrad K.P., and Umans J.J. The Normal and Diseased Kidney in Pregnancy. In: Diseases of the
Kidney and Urinary Tract: Eighth Edition. Volume 3, Chapter 74. Schrier R.W., editor. Lippincott Williams & Wilkens,
U.S.A., 2007.
Conrad K.P. Renal Function and Volume Homeostasis. In: Principles and Practice of Medical Therapy in Pregnancy,
4th edition. 2007. Gleicher N., ed. www.medicaltherapyinpregnancy.com.
Lindheimer M.D., Conrad K.P., and Karamanchi A.S. Renal Physiology and Disease in Pregnancy. In: The Kidney.
Physiology and Pathophysiology: Fourth Edition. Volume 2, Chapter 93. Seldin D.W., and Giebisch, G., editors.
Lippincott Williams & Wilkens, U.S.A., 2007.
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Jeyabalan A., Novak J., Shroff SG, and Conrad K.P. The vascular actions of relaxin. Adv Exp Med Biol. 612:65-87,
2007. (Or In: Agoulnik A.I. (editor). Relaxin and Related Peptides. Volume 612. Austin/New York: Landes
Bioscience/Springer, 2007:65-87).
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, in press.
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