Email:  jschafer@uab.edu
  Telephone: 205.934.7106
  Fax: 205.975.7679
  Bldg/Room: MCLM 832

Dr. James A. Schafer, Professor Emeritus, received his B.S. degree (1963) and his Ph.D. degree (1968) from the University of Michigan. He joined the faculty at UAB in 1970, following a teaching fellowship at the University of Michigan and postdoctoral fellowships at Gustav-Embden Center for Biochemistry in Frankfurt, Germany, and Duke University. Dr. Schafer received the second Robert F. Pitts Memorial Lectureship Award from the International Union of Physiological Sciences in 1983, The Homer W. Smith Award of the American Heart Association and the American Society of Nephrology in 1993, Max-Planck Prize of the Max-Planck Society and the von Humboldt Foundation of Germany in 1994, and the Carl W. Gottschalk Distinguished Lectureship Award of the American Physiological Society in 2001, all for excellence in renal physiology research. In 1995 he was elected to honorary membership in the American Society for Clinical Investigation. He has served as the editor of the American Journal of Physiology: Renal, Fluid & Electrolyte Physiology (1983-1989); as the secretary-treasurer of the American Society of Nephrology and Member of Council (1989-1992); and as the chairman of the Research Committee of the National Kidney and Urologic Diseases Advisory Board. Dr. Schafer is a past president of the American Physiological Society (1996-1997) and served as a Member of Council (1992-1998).  He also served on the Board, Executive Committee, and Public Affairs Executive Committee of the Federation of American Societies for Experimental Biology (FASEB, 1995-1999).

Research

Current research in our laboratory concerns the regulation of Na+ and water reabsorption, and K+ secretion, by the cortical collecting duct of the kidney. Of particular interest is the interaction of the two hormones that are the primary regulators of salt and water reabsorption in this segment: vasopressin (AVP or ADH) which is secreted by the posterior pituitary and aldosterone, a mineralocorticoid produced by the adrenal glands. We are also studying the effects of other autocoids in modulating the primary hormonal effects. Such autocoids include: epinephrine, norepinephrine, dopamine, natriuretic peptides, prostaglandins, and bradykinin. It appears that all of these substances ultimately regulate Na+ and water reabsorption, and K+ secretion, by determining the activity of corresponding channels in the luminal membrane of the collecting duct. Using physiological, biochemical, cellular and molecular biological approaches, we are examining the effects of dietary salt intake and genotype on the expression of autocoid receptor isoforms and their intracellular second messengers as an approach to understanding possible etiologies of salt-dependent hypertension. We are also studying the regulation of the trafficking of the epithelial Na⁺ channel that is regulated by these hormones and autocoids.  These studies use a surface labeling approach to determine the density of these channels in the apical  membrane of cultured epithelial cells that have been transfected with modified channels using retroviral methodology.

Selected Publications

1. Schafer JA, Andreoli TE, and Weinstein A. Milestones in Nephrology: Fluid absorption and active and passive flows in the rabbit superficial pars rects. J. Am. Soc. Nephrol. 11:784-800, 2000. [Original publication of Schafer et al. Am. J. Physiol.-Renal Physiol. 233:F154-F167, 1977 republished as part of the series "Milestones in Nephrology" with commentaries.]

2. Schafer JA.  Salt and water homeostasis:  Is it just a matter of good bookkeeping?  [Homer W. Smith Award Lecture at the American Society of Nephrology Meeting 1993.]  J. Am. Soc. Nephrol.   4: 1933-1950, 1994.

3. Morris RG, Tousson A, Benos DJ and Schafer JA.  Microtubule disruption prevents an AVP-stimulated chloride secretion but not sodium reabsorption in A6 cells.   Am. J. Physiol. 274: F300-F314, 1998.

4. Li, L and Schafer JA. Dopamine inhibits vasopressin-dependent cAMP production in the rat cortical collecting duct. Am. J. Physiol. 275: F62-F67, 1998.

5. Sun D, Wilborn TW and Schafer JA. Dopamine D4 receptor isoform mRNA and protein is expressed in the rat cortical collecting duct. Am. J. Physiol.44: F742-F751, 1998.

6. Schafer JA, Li L, Sun D, Morris RG and Wilborn, TW.  Regulation of amiloride-sensitive Na+ channels in the renal collecting duct.  Current Topics in Membranes, 47:109-131, 1999.

7. Schafer JA. Interaction of modeling and experimental approaches to understanding renal salt and water balance. Ann. Biomed. Eng. 28:1002-1009, 2000.

8. Yoder BK, Tousson A, Millican L, Wu JH, Bugg CE, Jr., Schafer JA, and Balkovetz DF. Polaris, a protein disrupted in orpk mutant mice is required for the assembly of renal cilium. Am. J. Physiol.-Renal Physiol. 2282:F541-F552, 2002.

9. Morris RG and Schafer JA. cAMP increases density of ENaC subunits in MDCK cells in direct proportion to amiloride-sensitive Na⁺ transport. J. Gen. Physiol. 120:71-85, 2002.

10. Schafer JA. Abnormal regulation of ENaC: syndromes of salt retention and salt wasting by the collecting duct. Am. J. Physiol.-Renal Physiol. 283:F221-F235, 2002.