Abstract

A high dietary potassium (K+) intake causes a rapid dephosphorylation and hence inactivation of the thiazide-sensitive NaCl cotransporter (NCC) in the renal distal convoluted tubule (DCT). Based on experiments in heterologous expression systems and in mice, it has been proposed that changes in plasma K+ concentrations ([K+]) modulate NCC phosphorylation via changes in intracellular Cl- concentrations that control the activity of the WNK/ SPAK kinase pathway. Using different ex-vivo systems namely isolated perfused mouse kidney, kidney slices and DCT microperfusion we demonstrate for the first time that plasma K+ directly modulate NCC phosphorylation in native DCT cells. Moreover, most prominent changes occur around physiological values of plasma [K+]. Data suggesting that NCC dephosphorylation upon increasing [K+] is independent of changes in intracellular [Cl-] and thus of the WNK / SPAK-OSR1 pathway will be discussed.     

About the speaker

David Penton Ribas, PhD

Institute of Anatomy,
University of Zurich,
Switzerland 

http://www.anatomy.uzh.ch/en/research/loffing/people/dpenton.html

Participation

The lecture is open to all and registration is not necesarry. Coffee and tea will be served.

Organiser and contact

Mads Vaarby Sørensen, AIAS Fellow
madssorensen@aias.au.dk

Phone: +4587153072

Aarhus Institute of Advanced Studies, AIAS

Høegh-Guldbergs Gade 6B
building 1630, 213
8000 Aarhus C
Denmark madssorensen