Divisiong of Nephrology and Hypertension




James McCormick, PhD.

James McCormick, PhD.
Assistant Professor of Medicine

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James McCormick, PhD.

Dr. McCormick completed his PhD in the laboratory of Dr. Jonathan Seckl in Edinburgh, UK. During his graduate work, he focused on transcriptional regulation of the glucocorticoid receptor, a key mediator of perinatal “programming” of adult diseases such as hypertension and dementia. He completed an American Heart Association-funded postdoctoral fellowship with Dr. David Pearce in the Division of Nephrology at UCSF, studying the physiological roles of serum and glucocorticoid-induced kinase (SGK) isoforms, and how they differentially regulate renal sodium transport. He joined the Division of Nephrology & Hypertension at OHSU in 2005. His current work uses mouse models to examine mechanisms of blood pressure regulation.


BSc (Honours), Biochemistry – University of Edinburgh, UK, 1996
PhD, Molecular Endocrinology – University of Edinburgh, UK, 2000


Postdoctoral Fellow, Nephrology – UCSF, 2000-2004

Research Interests:

Essential hypertension, defined as chronically elevated blood pressure occurring in the absence of identifiable causes, affects 25% of the adult population in the developed world and is a major independent risk factor for stroke, myocardial infarction, and congestive heart failure, as well as a major cause of end-stage renal disease.  At least 50% of hypertensive patients have a salt-sensitive component, and in approximately 30%, hypertension is predominantly due to abnormalities in renal sodium handling.  Although the bulk of filtered NaCl is reabsorbed by the proximal tubule, the thick ascending limb (TAL) and aldosterone-sensitive distal nephron (which includes the distal convoluted tubule (DCT), connecting segment, and collecting duct) play crucial roles in NaCl homeostasis.

Our major interest is the regulation of sodium transport along the TAL and DCT by kinases that activate sodium transporters including NKCC2 and NCC.  These kinases, the WNKs and SPAK/OSR1, have been identified as playing roles in hypertension in humans.  We recently identified a network of SPAK isoforms that interact to fine-tune sodium reabsorption.  Our future work aims to understand regulation of this network and how it ultimately affects blood pressure.  We use a broad variety of experimental techniques ranging from in vitro assays, through cell culture and whole animal physiology.  This allows us to integrate our findings to provide meaningful answers to whole body physiology.   

Representative Publications: