Susan Wall to Deliver Brenner Endowed Lectureship

Susan M. Wall

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Susan M. Wall, MD, will present the Barry M. Brenner Endowed Lectureship on Thursday, November 10. The topic of her presentation will be “Modulation of ENaC function by pendrin-dependent Cl-/HCO3- exchange.”

Dr. Wall is professor of medicine and physiology at Emory University School of Medicine in Atlanta. For the past 25 years, she has studied the renal physiology of H+/OH- transporters along the collecting duct.

The focus of her attention recently has been the renal physiology of the Cl-/HCO3- exchanger, pendrin. While pendrin’s critical role in hearing and thyroid function is well known, this transporter is also highly expressed in the apical regions of type B and non-A, non-B intercalated cells in the cortical collecting duct and connecting tubule, where it plays an important role in the renal regulation of blood pressure.

Dr. Wall and her colleagues have shown that pendrin mediates the absorption of chloride and the secretion of bicarbonate in the cortical collecting duct and that it is greatly upregulated by aldosterone, which stimulates chloride absorption and bicarbonate secretion in these segments. The researchers observed that in mice given a high-salt diet, in which circulating aldosterone concentration is low, blood pressure, serum electrolytes, and serum bicarbonate are similar in pendrin-null and wild-type mice. However, the pressor response to aldosterone is greatly blunted in pendrin-null mice, presumably due to the absence of pendrin-mediated chloride absorption. Moreover, when pendrin-null mice are changed from a high- to a low-sodium diet, they excrete more sodium and chloride than pair-fed wild-type mice. The chloriuresis observed in the salt-restricted pendrin-null mice could be readily explained by the absence of pendrin-mediated chloride absorption. However, because pendrin does not transport sodium, the researchers explored the cause of the natriuresis further. Although pendrin and the epithelial sodium channel (ENaC) localize to different cell types, Dr. Wall and her colleagues made the surprising observation that ENaC abundance and function are greatly reduced in pendrin-null mice. They demonstrated that pendrin modulates ENaC abundance and function in aldosterone-treated mice, at least in part by secreting bicarbonate into the luminal fluid, which stimulates ENaC abundance and function.

Dr. Wall received her undergraduate degree in chemistry from the University of Seattle and her MD from St. Louis University School of Medicine. She did her postgraduate medical training in internal medicine and nephrology at the University of California, Los Angeles, hospitals. She did research fellowships at UCLA and the National Heart, Lung, and Blood Institute. After a year on the faculty at the University of Texas Medical School at Houston, Dr. Wall moved to Emory in 2002.

Notes

[1] ASN gratefully acknowledges Monarch Pharmaceuticals for support of the Barry M. Brenner Endowed Lectureship.

October-November 2011 (Vol. 3, Number 10 & 11)