Short-term Regulation of Na+,K+-ATPase Activity by Dopamine

Publisher Website
Google Scholar
Abstract
The short term regulation of the activity of the Na,K-pump (Na+,K+-ATPase) is just beginning to be understood. By using single microdissected proximal tubule segments (PCT) (permeabilized in order to clamp Na entry), it was possible to study regulation of Na+,K+-ATPase activity in its own environment and in a well defined cell population. The Na+,K+-ATPase activity can be regulated over a short term via guanidine triphosphate (GTP) dependent regulatory proteins. However the guanidine proteins are not directly coupled to the Na,K-pump and the mechanism involves the activation of complex intracellular signalling system. Locally produced dopamine induces a dose dependent inhibition of Na+,K+ATPase activity. This inhibition is mediated by a complex mechanism that requires the activation of both membrane dopamine receptors, DA-1 and DA-2. It involves the activation of a pertussis toxin sensitive GTP-binding protein and activation of protein kinase C. A D A-2 agonist only inhibits Na+,K+-ATPase activity when it is incubated together with dibutyryl cAMP or Forskolin. We have therefore concluded that an increase in cellular cAMP levels plays a permissive role for DA-2 inhibition of Na+,K+-ATPase activity. A fully differentiated cell is required for dopamine inhibition of Na+,K+-ATPase activity. An abnormal regulation of proximal tubule Na+,K+-ATPase activity might be of importance in the pathogenesis of certain types of hypertension. Am J Hypertens 1990;3:51S-54S

This publication has 0 references indexed in Scilit: