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Mildred A Pointer

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Professor and Director
(919) 530-7016
(919) 530-6815
124 Julius L. Chambers Biomedical/Biotechnology Research Institute (BBRI)


Principal Investigator and Leader of the Pointer Research Enterprise (PRE, we put the "pre" in premier): provide vision and leadership to a brilliant team of junior investigators, research assistants, and trainees; provide an environment that fosters imagination and creativity; encourage growth and development for all members of PRE (investigators, staff, and students); and seek and procure independent funding for PRE.


My earliest research during my post-doctoral years at UNC under the mentorship of Drs. Carl Gottschalk and William Arendshorst examined the role of renal nerves in hypertension development. This was followed by my continued investigation of kidney and blood pressure regulation at Harvard with Dr. Victor Dzau showing that basal blood pressure is attributed to, in part, to atrial natriuretic protein effects. In subsequent years with Dr. Joseph Loscalzo at Harvard and Boston University, we made several key contributions to salt-sensitive hypertension: nitric oxide from inducible nitric oxide synthase is required for salt-sensitivity; and oxidative stress precedes impaired renal function associated with the hypertension.

Since establishing my own research program (Pointer Research Enterprise) at North Carolina Central University we have extended our study of the underlying mechanism of salt-sensitive hypertension. Our findings reveal that a) urinary excretion of calcium predicts the blood pressure rise in salt-sensitive hypertension; b) renal medullary calcium transport is the site of renal blood pressure regulation in salt-sensitive hypertension; and thiazide antihypertensive action is due, to a significant degree, to reduction in urinary calcium loss. We further showed that salt adds to the renal injury associated with hypertension and that stress exaggerates the toxic effect of salt. We have since added translational studies using cohorts of AAs. We show that the stress of racism contributes to resting blood pressure; anxiety state should be assessed when performing reactivity experiments; and prediabetic AA males have a 2.5 greater risk for renal injury compared to AA females.

We have established collaboration with Dr. Franceschini, research Associate Professor in Department of Epidemiology (UNC), and Dr. Elizabeth Hauser, Professor, Biostatistics and Bioinformatics, Center for the Study of Aging and Human Development; Director of Renal Genomics Core of the Duke O'Brien Center of Kidney Research (Duke) to extend our research on kidney disease in AAs to include the identification of genes that interact with stress to explain kidney disease disparity .

More recently, we have initiated a collaboration with Dr. Tim Wiltshire, Director of Pharmacogenomics and Individualized Therapy at UNC Eshelman School of Pharmacy at Chapel Hill. This initiative combines the Pointer and Wiltshire interest in salt-sensitive hypertension and how to improve treatment interventions.

1983-1986 Post-doctoral Fellow at UNC Chapel Hill
1986-1987 Post-doctoral Fellow Harvard Medical School
1987-1988 Research Fellow, Brigham and Women's Hospital, Boston, MA
1988-1991 Research Associate, Brigham and Women's Hospital, Boston, MA
1991-1993 Instructor in Medicine, Harvard Medical School and Brigham and Women's Hospital, Boston, MA
1994-2001 Research Assistant Professor in Medicine, Boston University School of Medicine, Boston, MA
2001- Associate Professor in Biology, North Carolina Central University
2001- Research Scientist in Biomedical/Biotechnology Research Institute, North Carolina Central University
2001- Adjunct Assistant Professor in Medicine, Duke University School of Medicine
2002-2003 Visiting Scholar in Department of Physics, Duke University
2005- Tenured
2016- Full professor

Research Interests

Mechanism of Salt-sensitive Hypertension
1. Salt-sensitive hypertension may be calcium-sensitive hypertension. We study the role of extracellular calcium in salt-sensitive hypertension.
2. Salt-sensitive hypertension may less to do with sodium chloride and more to do with potassium and calcium. We examine the interaction of potassium and calcium with salt consumption and excretion.

Biology of Stress and Kidney Disease
1. Stress exacerbates the effect of high salt on kidney injury independent of blood pressure.
2. Genetic predisposition is driven by exposure to environmental stress.
3. The biology of the stress and renal damage differs between males and females.
4. We have identified potential hormonal targets to explain the biology of stress-induced kidney injury.


PhD Wake Forest University 1983
BS North Carolina Central University 1974


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Selected Publications

1. Pointer, M. A., & Eley, S. , & Anderson, L. , & Brittany, W. (2015). Differential Effect of Renal Cortical and Medullary Interstitial Fluid Calcium on Blood Pressure Regulation in Salt-Sensitive Hypertension.. American Journal of Hypertension, 28, 1049-1055.
2. Pointer, M. A., & Hicks, K. , & Williams-Devane, C. , & Wells, C. (2015). Gender differences in preclinical markers of kidney injury in a rural north Carolina african-american cohort.. Frontiers in Public Health.
3. Pointer, M. A., & Daumerie, G. , & Bridges, L. , & Yancey, S. (2012). Physiological stress increases renal injury in eNOS-knockout mice.. Hypertension Research, 35, 318-324.
4. Pointer, M. A., & Yancey, S. , & Abou-Chacra, R. , & Petrusi, P. (2012). State Anxiety Is Associated with Cardiovascular Reactivity in Young, Healthy African Americans. International Journal of Hypertension.
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