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  • Jennifer M. Sasser, PhD


    Assistant Professor
    Office: G306
    Phone: (601) 984-1629
    E-mail: jsasser@umc.edu

    View CV


    Research interests

    • Cardiovascular and renal physiology and pharmacology
    • Potential therapeutic role of relaxin in hypertension and kidney disease
    • Renal adaptations to pregnancy and hypertension in pregnancy

    Current research

    My laboratory is interested in determining factors that lead to kidney disease during hypertension (high blood pressure) and identifying new targets for the treatment of these diseases. Previous work has shown that production of nitric oxide (NO) is decreased in chronic kidney disease, and this contributes to cardiovascular risk and to further progression of kidney damage. Therefore, interventions that can restore NO production are likely to reduce the cardiovascular complications of CKD as well as slow the rate of progression of renal injury.

    Our current work is focused on two main projects.  The goal of our first project is to test the therapeutic potential of relaxin in rodent models of kidney disease, specifically focusing on the effects of relaxin on the renal endothelin-NO pathway. Relaxin, a hormone that is increased in normal pregnancy, has been shown to cause vasodilation and increase renal blood flow via increased NO production. In addition, relaxin is also anti-fibrotic and may therefore improve kidney structure in disease states. In our second project, we have begun to examine the initiating causes of preeclampsia and the mechanisms by which the development of preeclampsia alters glomerular structure and function during pregnancy.

    Our laboratory has recently characterized the Dahl Salt Sensitive rat (on a 0.3% salt diet) as a model of preeclampsia that closely mimics the human disease. In addition to understanding the disease in pregnancy itself, we will also use this model to determine the effects of preeclampsia on the later development of cardio-renal disease in both the mother and the offspring. We use whole animal and molecular approaches including acute and chronic measurements of blood pressure and renal function and measures of protein abundance and activity.

    Selected publications

    • Gillis EE, Mooney JN, Williams JM, Garrett MR, Sasser JM. The Dahl Salt Sensitive rat on a normal salt diet is a spontaneous model of preeclampsia - comparison to Sprague Dawley and Spontaneously Hypertensive Rats.  Am J Physiol Regul Integr Comp Physiol, In press, 2015.
    • Sasser JM, Brinson KN, Tipton A, Sullivan JC.  Blood pressure, sex and female sex hormones influence renal inner medullary nitric oxide synthase activity and expression in Spontaneously Hypertensive Rats. Journal of the American Heart Association, In Press, 2015.
    • Sasser JM, Cunningham MC, Baylis C.  Relaxin reduces Oxidative Stress and Asymmetric Dimethylarginine in Angiotensin II Induced Hypertension.  Am J Physiol Renal Physiol, 307:F1355-62, 2014.
    • Sasser JM. The emerging role of relaxin as a novel therapeutic pathway in the treatment of chronic kidney disease. (Invited Review) Am J Physiol Regul Integr Comp Physiol. 305(6):R559-65, 2013.
    • Sasser, J. M., Akinsiku, O., Moningka, N. C., Jerzewski, K., Baylis, C., Leblanc, A. J., Kang, L. S., Sindler, A. L., and Muller-Delp, J. M. (2012) Sexual dimorphism in development of kidney damage in aging Fischer-344 rats, Gender medicine 9, 219-231. PubMed article   
    • Sasser, J. M., Moningka, N. C., Tsarova, T., and Baylis, C. (2012) Nebivolol does not protect against 5/6 ablation/infarction induced chronic kidney disease in rats - Comparison with angiotensin II receptor blockade, Life sciences 91, 54-63. PubMed article   
    • Sasser, J. M., Molnar, M., and Baylis, C. (2011) Relaxin ameliorates hypertension and increases nitric oxide metabolite excretion in angiotensin II but not N(omega)-nitro-L-arginine methyl ester hypertensive rats, Hypertension 58, 197-204. PubMed article   
    • Fekete, A., Sasser, J. M., and Baylis, C. (2011) Chronic vasodilation produces plasma volume expansion and hemodilution in rats: consequences of decreased effective arterial blood volume, American journal of physiology. Renal physiology 300, F113-118. PubMed article   
    • Sasser, J. M., Ni, X. P., Humphreys, M. H., and Baylis, C. (2010) Increased renal phosphodiesterase-5 activity mediates the blunted natriuretic response to a nitric oxide donor in the pregnant rat, American journal of physiology. Renal physiology 299, F810-814. PubMed article   
    • Sasser, J. M., Moningka, N. C., Cunningham, M. W., Jr., Croker, B., and Baylis, C. (2010) Asymmetric dimethylarginine in angiotensin II-induced hypertension, American journal of physiology. Regulatory, integrative and comparative physiology 298, R740-746. PubMed article  
    • Sasser, J. M., and Baylis, C. (2010) Effects of sildenafil on maternal hemodynamics and fetal growth in normal rat pregnancy, American journal of physiology. Regulatory, integrative and comparative physiology 298, R433-438. PubMed article  
    • Sasser, J. M., and Baylis, C. (2008) The natriuretic and diuretic response to dopamine is maintained during rat pregnancy, American journal of physiology. Renal physiology 294, F1342-1344. PubMed article   
    • Sasser, J. M., Sullivan, J. C., Hobbs, J. L., Yamamoto, T., Pollock, D. M., Carmines, P. K., and Pollock, J. S. (2007) Endothelin A receptor blockade reduces diabetic renal injury via an anti-inflammatory mechanism, Journal of the American Society of Nephrology : JASN 18, 143-154. PubMed article