Christopher T Banek, PhD

Summary

Throughout my career, I have focused on the physiological underpinnings of the etiology and treatment of high blood pressure (i.e. hypertension). While hypertension is a multi-faceted disease, I have focused my research primarily on neural (brain) and renal (kidney) contributions to the development and maintenance of hypertension. This was motivated, in part, by recent advancements in catheter-based targeted nerve ablation of renal nerves in humans, which mitigates or even reverses drug-resistant hypertension. While the anti-hypertensive effects are exciting, the mechanisms mediating the beneficial effects are unclear. Thus, our studies aim to elucidate the detailed mechanisms of renal nerves in hypertension and other renal diseases (polycystic kidney disease; ischemia-reperfusion injury; etc.) to provide a translational platform for development and refinement of emerging antihypertensive therapies. 

My recent work has differentiated between afferent (i.e. sensory) and sympathetic contributions to DOCA-salt model of hypertension through selective denervations, demonstrating the central role for afferent renal nerves in the disease etiology. My focus has now expanded to addressing the crucial questions of when and how changes in renal nerve activity modulate arterial pressure control. Using a combination of telemetry-based measurements and molecular interrogation, we are currently leveraging this unique experimental approach to elucidate the physiological relationship between changes in renal afferent nerve activity and hypertension-induced renal inflammation and the concomitant autonomic dysfunction. 

Our current and previous work in hypertension and renal disease has laid the groundwork for expanding these findings to other renal disease models such as polycystic kidney disease (PKD). We have recently published on the differential contribution of renal sympathetic and afferent nerves in ARPKD development, which highlighted the specific role for afferent renal nerves in driving the cystogenesis in a rat model of PKD. Our current studies are now focused on the molecular drivers of increased afferent nerve activity in our PKD model, as well as the temporal relationship between afferent renal nerve activity changes and the primary drivers of ARPKD development.

Current Research Funding:

• R00HL141650, National Institutes of Health (NHLBI), Project Title: Renal Denervation to Treat Hypertension: Mechanisms and Mediators
• U24DK126110, National Institutes of Health (NIDDK), Pilot and Feasibility Award. Project Title: Autosomal Recessive Polycystic Kidney Disease Progression: Role of Renal Autonomic Dysregulation
• 1022534, Polycystic Kidney Disease Foundation, PKD Research Grant, Project Title: Renal Innervation and Nerve Activity Influence on Cystic Progression in ARPKD 
• University of Arizona COM-T FUTURRE Award

Recent Publications:

1. Gauthier MM, Parvin I, Dennis M, Morales M, Banek CT. Contribution of Afferent Renal Nerves to Cystogenesis and Arterial Pressure Regulation in a Preclinical Model of Autosomal Recessive Polycystic Kidney Disease. 2022. Am J Physiol Renal Physiol. 322(6):F680-F691.
2. Banek CT, Bradshaw JL, Coats LE, Alexander BT, and Goulopoulou S. 2021. Getting It Right: Preventing Drift in Baseline Cardiovascular Phenotype When Using Sprague Dawley Rats. Am J Physiol Heart and Circ. 321(3):H475-H478.
3. Geisler CE, Ghimire S, Hepler C, Miller KE, Bruggink SM, Kentch KP, Higgins MR, Banek CT, Yoshino J, Klein S, Renquist BJ. 2021. Hepatocyte membrane potential regulates serum insulin and insulin sensitivity by altering hepatic GABA release. Cell Reports. 35(13), 109298.
4. Asirvatham-Jeyaraj N, Gauthier MM, Banek CT, Ramesh A, Burnett R, Garver H, Van Helden D, Fink GD, Osborn JW. 2020. Renal denervation and celiac ganglionectomy decrease mean arterial pressure similarly in genetically hypertensive BPH/2J mice. Hypertension. 77(2):519-528.
5. Banek CT, Gauthier MM, Van Helden D, Fink GD, Osborn JW. 2019. Renal Inflammation in DOCA-Salt Hypertension: Role of Renal Nerves and Arterial Pressure. Hypertension. 73(5):1079-1086.
6. Kiuchi MG, Esler MD, Fink GD, Osborn JW, Banek CT, Böhm M, Denton KM, DiBona GF, Everett TH, Grassi G, Katholi RE, Knuepfer MM, Kopp UC, Lefer DJ, Lohmeier TE, May CN, Mahfoud F, Paton JFR, Schmieder RE, Pellegrino PR, Sharabi Y, Schlaich MP. 2019. Proceedings from the International Sympathetic Nervous System (SNS) Summit 2018: Focus on Renal Denervation. J Am Coll Cardiol. 18;73(23):3006-3017.
7. Collister JP, Nahey DB, Hartson R, Wiedmeyer CE, Banek, CT, and Osborn JW. 2018. Lesion of the OVLT markedly attenuates chronic deoxycorticosterone acetate (DOCA) salt hypertension in the rat. Am J Physiol Regul Integr Comp Physiol. 315(3):R568-R575.
8. Banek CT, Gauthier MM, Baumann DC, Van Helden D, Asirvatham-Jeyaraj N, Panoskaltsis-Mortari A, Fink GD, Osborn JW. 2018. Targeted Afferent Renal Denervation Reduces Arterial Pressure but not Renal Inflammation in Established DOCA-salt Hypertension in the Rat. Am J Physiol Regul Integr Comp Physiol. 314(6):R883-91.
9. Osborn JW, Banek CT. 2018. Device-Based Renal Denervation as a Novel Hypertension Therapy: Lost, and Then Found, in Translation? Hypertension. 71(3): 383-388.
10. Banek CT, Knuepfer MM, Foss JD, Fiege JK, Asirvatham-Jeyaraj N, Van Helden D, Shimizu Y, Osborn JW. 2016. Resting afferent renal nerve discharge and renal inflammation: Elucidating the role of afferent and efferent renal nerves in DOCA-salt hypertension. Hypertension. 68(6):1415-23.