Nathan Grainger

Nathan Grainger serves as a Research Assistant Professor in the Department of Physiology and Cell Biology at the University of Nevada, Reno, where his laboratory investigates fundamental mechanisms of pacemaker function in cardiac and urinary systems.

His academic credentials include a B.Sc. in Neuroscience from the University of Manchester, United Kingdom, and a Ph.D. in Cellular and Molecular Pharmacology and Physiology from the University of Nevada, Reno.

Dr. Grainger's primary research explores the autonomic regulation of sinoatrial node vasculature, energy metabolism in pacemaker cells, and pathophysiological mechanisms in heart failure. His work bridges cardiac electrophysiology and vascular biology, with significant focus on microvascular rarefaction, mitochondrial-sarcoplasmic reticulum interactions, and regional heterogeneity in nodal tissue. Additionally, he investigates peristaltic pacemaker mechanisms in the renal pelvis, examining ion channel dynamics and interstitial cell function.

Analysis of his 15 most recent publications reveals a cohesive research trajectory centered on pacemaker dysfunction across organ systems. His cardiac studies predominantly address sinoatrial node vulnerability in heart failure (including HFpEF), while urological work emphasizes Ca²⁺-activated chloride channels and T-type calcium channels in urinary tract pacemaking. This dual focus demonstrates how cellular energy regulation and vascular control mechanisms underlie rhythmicity in both heart and urinary systems.

Dr. Grainger leads an active research laboratory utilizing advanced techniques including vibratome sectioning for live imaging of intact pacemaker regions, molecular channel analysis, and metabolic studies. His team develops innovative approaches to isolate and characterize pacemaker tissues while investigating translational implications for heart failure and urinary motility disorders.