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  • Jennifer M. Sasser, PhD

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

    Research interests

    • Cardiovascular and renal physiology and pharmacology
    • Potential therapeutic role of relaxin in hypertension and kidney disease
    • Renal adaptations to 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.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.The current goal of the laboratory 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ーNO pathway. 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

    • 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   
    • Chen, G. F., Moningka, N. C., Sasser, J. M., Zharikov, S., Cunningham, M., Jr., Tain, Y. L., Schwartz, I. F., and Baylis, C. (2012) Arginine and asymmetric dimethylarginine in puromycin aminonucleoside-induced chronic kidney disease in the rat, American journal of nephrology 35, 40-48. PubMed article   
    • Moningka, N. C., Tsarova, T., Sasser, J. M., and Baylis, C. (2012) Protective actions of nebivolol on chronic nitric oxide synthase inhibition-induced hypertension and chronic kidney disease in the rat: a comparison with angiotensin II receptor blockade, Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association 27, 913-920. 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   
    • Kirabo, A., Kearns, P. N., Jarajapu, Y. P., Sasser, J. M., Oh, S. P., Grant, M. B., Kasahara, H., Cardounel, A. J., Baylis, C., Wagner, K. U., and Sayeski, P. P. (2011) Vascular smooth muscle Jak2 mediates angiotensin II-induced hypertension via increased levels of reactive oxygen species, Cardiovascular research 91, 171-179. PubMed article   
    • Moningka, N. C., Sasser, J. M., Croker, B., Carter, C., and Baylis, C. (2011) Protection against age-dependent renal injury in the F344xBrown Norway male rat is associated with maintained nitric oxide synthase, Mechanisms of ageing and development 132, 1-7. 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   
    • Chen, G. F., Wagner, L., Sasser, J. M., Zharikov, S., Moningka, N. C., and Baylis, C. (2010) Effects of angiotensin type 1 receptor blockade on arginine and ADMA synthesis and metabolic pathways in fawn-hooded hypertensive rats, Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association 25, 3518-3525. 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  
    • Boesen, E. I., Sasser, J. M., Saleh, M. A., Potter, W. A., Woods, M., Warner, T. D., Pollock, J. S., and Pollock, D. M. (2008) Interleukin-1beta, but not interleukin-6, enhances renal and systemic endothelin production in vivo, American journal of physiology. Renal physiology 295, F446-453. 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   
    • Kang, K. T., Sullivan, J. C., Sasser, J. M., Imig, J. D., and Pollock, J. S. (2007) Novel nitric oxide synthase--dependent mechanism of vasorelaxation in small arteries from hypertensive rats, Hypertension 49, 893-901. 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