Renal Inflammation in DOCA-Salt Hypertension: Role of Renal Nerves and Arterial Pressure. Banek CT, Gauthier MM, Van Helden D, Fink GD, Osborn JW.Renal denervation and celiac ganglionectomy decrease mean arterial pressure similarly in genetically hypertensive BPH/2J mice. Asirvatham-Jeyaraj N, Gauthier MM, Banek CT, Ramesh A, Burnett R, Garver H, Van Helden D, Fink GD, Osborn JW.Hepatocyte membrane potential regulates serum insulin and insulin sensitivity by altering hepatic GABA release. Geisler CE, Ghimire S, Hepler C, Miller KE, Bruggink SM, Kentch KP, Higgins MR, Banek CT, Yoshino J, Klein S, Renquist BJ.Getting It Right: Preventing Drift in Baseline Cardiovascular Phenotype When Using Sprague Dawley Rats. Banek CT, Bradshaw JL, Coats LE, Alexander BT, and Goulopoulou S.Contribution of Afferent Renal Nerves to Cystogenesis and Arterial Pressure Regulation in a Preclinical Model of Autosomal Recessive Polycystic Kidney Disease. Gauthier MM, Parvin I, Dennis M, Morales M, Banek CT.University of Arizona COM-T FUTURRE Award.1022534, Polycystic Kidney Disease Foundation, PKD Research Grant, Project Title: Renal Innervation and Nerve Activity Influence on Cystic Progression in ARPKD.Project Title: Autosomal Recessive Polycystic Kidney Disease Progression: Role of Renal Autonomic Dysregulation U24DK126110, National Institutes of Health (NIDDK), Pilot and Feasibility Award.R00HL141650, National Institutes of Health (NHLBI), Project Title: Renal Denervation to Treat Hypertension: Mechanisms and Mediators.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. 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 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). 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. My focus has now expanded to addressing the crucial questions of when and how changes in renal nerve activity modulate arterial pressure control. 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 recent work has differentiated between afferent (i.e. 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. While the anti-hypertensive effects are exciting, the mechanisms mediating the beneficial effects are unclear. 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 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. Throughout my career, I have focused on the physiological underpinnings of the etiology and treatment of high blood pressure (i.e.
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