Meredith Hay
Professor, BIO5 Institute
Professor, Evelyn F Mcknight Brain Institute
Professor, Physiology
Professor, Psychology
Professor, Physiological Sciences - GIDP
Primary Department
Department Affiliations
(520) 626-7384
Work Summary
Our lab is focused on the development of novel peptides to inhibit this inflammatory cascade and improve brain blood flow. These peptides are designed to significantly improve serum half-life and penetrate the blood-brain-barrier. These peptides act to inhibit the inflammatory pathways at both the level of brain blood vessels and the brain itself.
Research Interest
Dr. Hay is internationally known for her work in cardiovascular neurobiology and her current studies on the role of sex and sex hormones in the development of hypertension. She has been continuously funded by the NIH and other sources for the past 26 years. She has extensive experience in central renin angiotensin mechanisms, neurophysiology and reactive oxygen and cytosolic calcium neuroimaging and in advancing knowledge related to central mechanisms of neurohumoral control of the circulation. She is a Professor of Physiology at the University of Arizona College of Medicine and maintains active participation in the American Physiological Society, the Society of Neuroscience, AAAS, and has served on numerous editorial boards of prestigious scientific journals and grant review panels for the National Institutes of Health and the National American Heart Association. The primary focus of Dr. Hay’s laboratory is the understanding of the biophysical and cellular mechanisms underlying neurotransmitter modulation of sympathetic outflow and ultimately arterial blood pressure. The scientific questions being asked are: 1) What central neurotransmitter mechanisms are involved in the normal regulation of cardiovascular function? 2) Does the development of some forms of hypertension involve biophysical or molecular alteration in the neurotransmitter mechanisms regulating cardiovascular control? 3) Can these central signal transduction systems, which control sympathetic outflow and ultimately arterial blood pressure, be altered in order to prevent or attenuate the development of some forms of hypertension? 4) Are there gender related differences in some of these mechanisms?Dr. Hay has extensive national experience in university-wide administration and interdisciplinary research program development. Prior to coming to the University of Arizona in 2008 as Executive Vice President and Provost, Dr. Hay was the Vice President for Research for the University of Iowa, where she worked with state and federal lawmakers, private sector representatives, and local community groups to broaden both private and public support for research universities. Dr. Hay, a Texas native, earned her B.A. in psychology from the University of Colorado, Denver, her M.S. in neurobiology from the University of Texas at San Antonio, and her Ph.D. in cardiovascular pharmacology from the University of Texas Health Sciences Center, San Antonio. She trained as a postdoctoral fellow in the Cardiovascular Center at the University of Iowa College of Medicine and in the Department of Molecular Physiology and Biophysics at Baylor College of Medicine in Houston. She was a tenured faculty member of the University of Missouri-Columbia from 1996-2005. Prior to Missouri, she was a faculty member in the Department of Physiology at the University of Texas Health Science Center- San Antonio.

Publications

Hay, M., Vanderah, T. W., Samareh-Jahani, F., Constantopoulos, E., Uprety, A. J., & Barnes, C. A. (2017). Cognitive impairment in heart failure: A protective role for Angiotensin-(1-7). Behavioral Neuroscience, 131, 99-114.
BIO5 Collaborators
Carol A Barnes, Meredith Hay
Pollow, D. P., Uhrlaub, J., Romero-Aleshire, M. J., Sandberg, K., Nikolich-Zugich, J., Brooks, H. L., & Hay, M. (2014). Sex differences in T-lymphocyte tissue infiltration and development of angiotensin II hypertension. Hypertension, 64(2), 384-90.
BIO5 Collaborators
Heddwen L Brooks, Meredith Hay

There is extensive evidence that activation of the immune system is both necessary and required for the development of angiotensin II (Ang II)-induced hypertension in males. The purpose of this study was to determine whether sex differences exist in the ability of the adaptive immune system to induce Ang II-dependent hypertension and whether central and renal T-cell infiltration during Ang II-induced hypertension is sex dependent. Recombinant activating gene-1 (Rag-1)(-/-) mice, lacking both T and B cells, were used. Male and female Rag-1(-/-) mice received adoptive transfer of male CD3(+) T cells 3 weeks before 14-day Ang II infusion (490 ng/kg per minute). Blood pressure was monitored via tail cuff. In the absence of T cells, systolic blood pressure responses to Ang II were similar between sexes (Δ22.1 mm Hg males versus Δ18 mm : Hg females). After adoptive transfer of male T cells, Ang II significantly increased systolic blood pressure in males (Δ37.7 mm : Hg; P

Ji, H., Zheng, W., Li, X., Liu, J., Wu, X., Zhang, M. A., Umans, J. G., Hay, M., Speth, R. C., Dunn, S. E., & Sandberg, K. (2014). Sex-specific T-cell regulation of angiotensin II-dependent hypertension. Hypertension, 64(3), 573-82.

Studies suggest T cells modulate arterial pressure. Because robust sex differences exist in the immune system and in hypertension, we investigated sex differences in T-cell modulation of angiotensin II-induced increases in mean arterial pressure in male (M) and female (F) wild-type and recombination-activating-gene-1-deficient (Rag1(-/-)) mice. Sex differences in peak mean arterial pressure in wild-type were lost in Rag1(-/-) mice (mm Hg: wild-type-F, 136±4.9 versus wild-type-M, 153±1.7; P

Hay, M., & Bishop, V. S. (1991). Effects of area postrema stimulation on neurons of the nucleus of the solitary tract. The American journal of physiology, 260(4 Pt 2), H1359-64.

Previous studies have suggested that neurons of the area postrema may modulate cardiovascular function through an interaction at the level of the nucleus of the solitary tract (NTS). Using an in vitro brain slice preparation of the rabbit medulla, the present study investigated the electrophysiological and pharmacological effects of area postrema stimulation on NTS neuronal activity. In the majority of neurons tested (85.7%), electrical stimulation of the area postrema consistently produced either single or multiple action potentials in NTS neurons. Latency values for neurons showing single spike responses to area postrema stimulation ranged from 3.0 to 17.0 ms with an average latency of 9.3 +/- 4.3 ms. The average threshold for area postrema activation of these nonspontaneously active NTS neurons was 99.8 +/- 12 microA with a stimulus threshold range between 15 and 200 microA (n = 53). Perfusion of the slice with phentolamine (1.0 microM) or yohimbine (200 nM) blocked the area postrema-evoked action potentials, whereas perfusion of the slice with prazosin (200 nM) had no effect. These findings suggest that area postrema neurons do modulate NTS neuronal activity and that this modulation results in an increase in NTS neuronal activation.

Cox, B. F., Hay, M., & Bishop, V. S. (1990). Neurons in area postrema mediate vasopressin-induced enhancement of the baroreflex. The American journal of physiology, 258(6 Pt 2), H1943-6.

Intravenous infusion of arginine vasopressin (AVP) has been shown to enhance baroreflex sensitivity, and this enhancement is dependent on the integrity of the area postrema. However, previous studies did not differentiate a role for cell bodies in the area postrema vs. the dense network of fibers located in and around the lateral and ventral margins of this circumventricular organ. In the present study, baroreflex function was assessed in conscious rabbits by examining heart rate after ramp infusions of phenylephrine (PE) and AVP. The subsequent day, the excitotoxin kainic acid was injected (30 nl initially, with five 15-nl supplemental injections of a 1 ng/nl solution over 1 h) into the area postrema, thus selectively destroying cell bodies. After an 8-day recovery period, baroreflex function was again assessed. The bradycardic response to graded infusion of PE (slope = -2.29 +/- 0.30) was not significantly different after selective lesions of area postrema neurons (slope = -1.88 +/- 0.49). In contrast, the previously enhanced bradycardic response to infusion of AVP (slope = -5.76 +/- 1.02) was significantly attenuated (slope = -2.31 +/- 0.21) to levels similar to that seen with infusion of PE. Thus selective chemical lesions of area postrema neurons block vasopressin-induced enhancement of the baroreflex.