Steven C. Sansom

Steven C. SansomProfessor
Ph.D. from University of Texas Health Science Center at Houston, 1984
Major Interest: Renal Physiology
Specialty: Renal Ion Transport
Curriculum Vitae

The diet of ancient man consisted of a high K, low Na content obtained from fruits, vegetables and roots.  Except for some indigenous peoples of Africa and South America, we have switched our diet to a content of high Na and Low K.  It is been known for several years, however, that the high K diet is highly associated with reduced stroke and cardiovascular disease.

Potassium is beneficial and necessary for our health; however, plasma K must be maintained within very narrow limits for the proper functioning of our heart , muscles and nerves.  We are able to maintain physiological normal plasma K concentration after consuming large quantities of dietary K.  However, our plasma K concentration can increase to extremely high values with a crush injury and can be reduced to dangerously low values when taking diuretic agents designed to reduce blood pressure.  For these reasons, it is very  important to understand fully the mechanisms by which the kidneys adapt slowly to a high K dietary intake and how K can be eliminated during a sudden elevation as occurs with a crush injury. 

Our laboratory has discovered two types of potassium channels that are involved in handling a high K diet.  The first channel (BK-α/β1) is comprised of an alpha subunit (BK-α) and an ancillary beta1 subunit (BK-β1) and is located in distal nephron principal cells, known for reabsorbing Na in exchange for secreted K.  We found that mice with a genetic knock-out of the BK-β1 subunit are unable to excrete K as well as wild types when consuming a high K diet.  Deficient K secretion causes aldosteronism, which results in retention of K, Na, Cl and water leading to an increase in mean arterial blood pressure.

The second channel, the BK-α/β4, resides in intercalated cells, known for acid-base transport in the distal nephron.  Our laboratory has discovered that mice with a knock-out of the BK-β4 are unable to maintain K balance when consuming a low Na, high K diet.  K secretion in the absence of Na reabsorptive exchange (Na-independent K secretion) was prevalent with ancient man and is still evident in the Yamamoto tribes in South America; however, the mechanism has not been understood.  Our goal is to determine the role of the BK-α/β4 channel during Na-independent K excretion.

Figure A shows a single cortical collecting duct from mouse on control diet with co-immunohistochemical staining of BK-a subunit (red) on intercalated cells (arrow) and aquaporin 3 (green), a marker of the basolateral membrane of principal cells. BK channels are cytoplasmic with a control diet and appear apically with high aldosterone and alkaline conditions. B. Shows a patch clamp recording of two BK channels of cortical collecting ducts (arrow at closed state).    

 Recent publications:

  1. Wen, D., Cornelius, R.J., Rivero-Hernandez, D., Yuan, Y., Li, H. Ph.D.1, Weinstein, A.M. and S. C. Sansom. Relation between BK-a/b4-mediated K secretion and ENaC-mediated Na reabsorption. Kidney International. 2014, 86: 139-145. PMID:24573316
  2. Cornelius, R.J., Wen, D., Li, H., Yuan, Y. Wang-France, J., Warner, P.C. and S.C. Sansom. Low Na, high K diet and the role of aldosterone in BK-mediated K excretion. PLoS One. 2015 10 (1) e0115515. PMID:25607984
  3. Wen, D., Yuan, Y., Warner, P.C., Wang, B., Cornelius, R.J., Wang-France, J., Li, H., Boettger, T., and S. C. Sansom.. Increased ENaC activity contributes to hypertension caused by NBCe2 deficiency. Hypertension. 2015. 66 (1) 68-74. PMID:25941340
  4. Wen, D., Yuan, Y., Cornelius, R.J., Li, H., Warner, P.C, Wang, B., Wang-France, J., Boettger, T. and S.C. Sansom. Deficient acid handling with distal RTA in the NBCe2 knockout mouse. AJP: Renal, 2015. 309 (6) 523-530 PMID:26109087
  5. Cornelius, R.J., Wang, B., Wang-France, J., and S.C. Sansom. Maintaining K balance on the low Na, high K diet. AJP: Renal, 2016. 310 (7) 581-595 PMID:26739887