Heddwen Brooks

Research Interests

Our research goals are to understand how kidney function is regulated by the anti-diuretic hormone, vasopressin and the steroid hormone, estrogen. We focus on diabetes, lithium-induced diabetes insipidus and polycystic kidney disease (PKD)
Find out more about our research at the following links

Brooks Lab on Arizona Illustrated, KUAT
Brooks Lab in UA News
Focus on Faculty: Dr Brooks
Dr Brooks UA Leadership Institute Fellow


Kidney and Diabetes Research in the Brooks Lab
Diabetes, congestive heart failure and poly-cystic kidney disease are diseases that have been associated with defects in the handling of salt and water by the kidney. Common in individuals with these disorders are elevated circulating levels of vasopressin, the peptide hormone that regulates renal water excretion. Circulating vasopressin plays a critical role in extra-cellular fluid expansion and development of hypertension, thus contributes to the pathogenesis of the disease.
Vasopressin has clear long-term actions in the kidney, associated with regulatory processes at a transcriptional level as demonstrated by vasopressin-induced increases in aquaporin-2 transcription and translation. Circulating vasopressin also increases the concentrating capacity of the renal medulla by activating the counter current mechanism. The result is an increase in medullary osmotic stress that can directly activate renal cell signaling pathways and gene transcription. Thus specific effects of vasopressin on gene expression are not delineated from secondary alterations associated with this change in medullary osmolality.
This is clinically important as patients with diabetes, heart failure and polycystic kidney disease have high levels of circulating vasopressin, yet when they are treated with diuretics to reduce hypertension, have a decreased renal function and local osmolality.
Research Projects
1) Vasopressin and Renal Cell Proliferation: In Polycystic Kidney Disease (PKD) and in lithium-induced nephrogenic diabetes insipidus (NDI), epithelial cells of the kidney proliferate and renal function is reduced. Vasopressin receptor pathways have been targeted as pharmacological interventions for PKD and they reduce cyst formation and proliferation. We are interested in the mechanisms that trigger collecting ducts to proliferate. We use in vivo and in vitro models to study renal cell proliferative pathways.2) Vasopressin and ER Stress: We are investigating the role that ER stress plays to pre-condition renal medullary cells from entering apoptosis following osmotic stress, and in the regulation of AQP2 trafficking to the membrane. We recently identified a urea-induced cell stress activation involving the phosphorylation of eIF2alpha via the kinase GCN2.
3) Diabetes, Menopause and Metabolic Syndrome: We are studying how sex differences effect the onset of metabolic syndrome and diabetes, focusing on diabetic kidney disease and renal function. Specifically we are identifying the role that the steroid hormones testosterone and estrogen have on glucose impairment, insulin resistance, in addition to their effect on renal salt and water transport, and regulation of extracellular fluid balance.
Courses Taught
Fall: PSIO 503 Cellular and Molecular PhysiologySpring: PSIO 603 Systems Physiology (Course Coordinator) Spring: AZMED CPRSpring: AZMED Advanced TopicsDr Brooks is currently serving as Chair of the Renal Section of the American Physiological Society, serves on the VA Nephrology Review Panel, and is an author of the textbook "Ganong’s Review of Medical Physiology", 23rd edition