Sathish Kumar, DVM, PhD

Associate Professor
Comparative Biosciences
3256 Veterinary Building
2015 Linden Dr
Madison, WI 53706
Focus Groups: 
Signal Transduction
PhD, Indian Veterinary Research Institute, India
DVM, Madras Veterinary College, India
Research Summary: 
Physiological and pathophysiological mechanisms underlying blood pressure regulation and hypertension. Fetal origins of hypertension and diabetes. Sex differences in vascular and metabolic function.
Research Detail: 

A woman’s body undergoes many changes at the onset of pregnancy. The most profound effects are observed in the cardiovascular system where blood volume increases by 50%, heart rate increases by 10-15 beats per minute, cardiac output increases by 30-50%, blood pressure decreases by 10-15 mm Hg, and hematocrit level decreases. These physiologic changes are essential to meet the nutritional and metabolic demands of her developing fetus. Hypertensive disorder of pregnancy, called preeclampsia, occur when these cardiovascular adjustments fail to reach optimal levels. A pregnant woman’s daily environment — the air she breathes, the food and drink she consumes, her weight and fitness, the chemicals and infections she is exposed to, even the emotions she feels — is shared in some fashion with her fetus. When the mother develops hypertension, the fetus responds by undergoing what is called “programming” whereby the fetus modifies its gene expression in way that will give them a survival advantage. In the long run, these modifications are in fact not advantageous, and have been found to lead to hypertension and diabetes during adulthood. These programming effects differ between male and female fetuses and activate sex-specific hypertensive and/or diabetic mechanisms. Our laboratory is interested in understanding the physiological and pathophysiological mechanisms underlying blood pressure control during pregnancy and the fetal origins of adult hypertension and diabetes. We use an integrated approach that combines basic science, molecular laboratory techniques, and state-of-the-art cardiovascular tools to study:

a)      The mechanisms that contribute to normal cardiovascular adaptations to pregnancy -- with focus on steroid hormones and renin-angiotensin system.

b)      Why these cardiovascular changes are perturbed in some pregnant women, and if lifestyle choices and disease(s) during pregnancy (i.e. endocrine disruption, stress, smoking, drinking alcohol, hypoxia, infection, etc.) play a role.

c)      How disorders in the mother induce organizational and structural changes in the heart and vasculature of the fetus -- with a focused look at the roles of adrenal and gonadal hormones, genes, and inflammatory factors.

d)      How the mechanisms of hypertension and diabetes differ between males and females with focus on the endothelium and vascular smooth muscle signaling.

An understanding of these pregnancy and fetal mechanisms will help to prevent abnormal maternal vascular function and the consequent development of adult diseases. This study provides a novel approach to bring preventive medicine into the womb. Further, understanding the sex effects in hypertension and diabetes will provide knowledge for the development of sex-specific treatments for these disorders.

Selected Publications: 
Elevated Testosterone Reduces Uterine Blood Flow, Spiral Artery Elongation, and Placental Oxygenation in Pregnant Rats. Gopalakrishnan K, Mishra JS, Chinnathambi V, Vincent KL, Patrikeev I, Motamedi M, Saade GR, Hankins GD, Sathishkumar K. Hypertension (Dallas, Tex. : 1979). 2016; 67(3):630-9. PMID: 26781277
Prenatal testosterone exposure induces hypertension in adult females via androgen receptor-dependent protein kinase Cδ-mediated mechanism. Blesson CS, Chinnathambi V, Hankins GD, Yallampalli C, Sathishkumar K. Hypertension (Dallas, Tex. : 1979). 2015; 65(3):683-690. PMID: 25489059
Elevated testosterone levels during rat pregnancy cause hypersensitivity to angiotensin II and attenuation of endothelium-dependent vasodilation in uterine arteries. Chinnathambi V, Blesson CS, Vincent KL, Saade GR, Hankins GD, Yallampalli C, Sathishkumar K. Hypertension (Dallas, Tex. : 1979). 2014; 64(2):405-14. PMID: 24842922
Gestational exposure to elevated testosterone levels induces hypertension via heightened vascular angiotensin II type 1 receptor signaling in rats. Chinnathambi V, More AS, Hankins GD, Yallampalli C, Sathishkumar K. Biology of reproduction. 2014; 91(1):6. PMID: 24855104
Prenatal testosterone induces sex-specific dysfunction in endothelium-dependent relaxation pathways in adult male and female rats. Chinnathambi V, Yallampalli C, Sathishkumar K. Biology of reproduction. 2013; 89(4):97. PMID: 23966325
Calcitonin gene-related family peptides in vascular adaptations, uteroplacental circulation, and fetal growth. Yallampalli C, Chauhan M, Sathishkumar K. Current vascular pharmacology. 2013; 11(5):641-54. PMID: 24063381
Testosterone alters maternal vascular adaptations: role of the endothelial NO system. Chinnathambi V, Balakrishnan M, Ramadoss J, Yallampalli C, Sathishkumar K. Hypertension (Dallas, Tex. : 1979). 2013; 61(3):647-54. PMID: 23339170
Hyperandrogenemia reduces endothelium-derived hyperpolarizing factor-mediated relaxation in mesenteric artery of female rats. Mishra JS, More AS, Hankins GDV, Kumar S. Biology of reproduction. 2017; 96(6):1221-1230. PMID: 28486649
Fetal sex-related dysregulation in testosterone production and their receptor expression in the human placenta with preeclampsia. Sathishkumar K, Balakrishnan M, Chinnathambi V, Chauhan M, Hankins GD, Yallampalli C. Journal of perinatology: official journal of the California Perinatal Association. 2012; 32(5):328-35. PMID: 21904298
Postnatal Cardiovascular Consequences in the Offspring of Pregnant Rats Exposed to Smoking and Smoking Cessation Pharmacotherapies. Gopalakrishnan K, More AS, Hankins GD, Nanovskaya TN, Kumar S. Reproductive sciences (Thousand Oaks, Calif.). 2017; 24(6):919-933. PMID: 27733658