de Silva, H.A.Carver, J.G.Aronson, J.K.2014-10-292014-10-291996Clinical Science. 1996; 91(6): pp.725-7310143-5221 (Print)1470-8736 (Electronic)http://repository.kln.ac.lk/handle/123456789/1278Indexed in MEDLINENa+/K+/2Cl- co-transport mediates a bidirectional symport of Na+, K+ and Cl-. The important properties of the co-transport system are its requirement for Na+, K+ and Cl- and its inhibition by loop diuretics such as bumetanide. This co-transporter has been described in a number of animal and human tissues. However, its presence in human platelets, although inferred, has not been demonstrated directly. 2. We have studied the efflux of 86Rb+ (a marker for K+) from Rb(+)-loaded platelets, and have defined their response to stimulation by high concentrations of external K+. 3. KCl (30-120 mmol/l) stimulated a concentration-dependent increase in 86Rb+ efflux from the platelets. This efflux was completely inhibited by bumetanide (10 mumol/l) but was insensitive to ouabain and R(+)-[(dihydroindenyl)oxy]alkanoic acid. It also required Cl- in the external medium, but did not depend on the presence of extracellular Na+. 4. These observations suggest that 86Rb+ efflux from platelets stimulated by external K+ occurs via Na+/K+/2Cl- co-transport acting in a K+/K+ (K+/Rb+) exchange mode. 5. Non-stimulated efflux of 86Rb+ from the platelets (i.e. in the presence of 5 mmol/l K+) had the characteristics of Na+/K+/2Cl- co-transport acting in normal mode.Biological Transport-drug effectsBlood Platelets-metabolismBumetanide-pharmacologyCarboxylic Acids-pharmacologyChlorine-bloodIndenes-pharmacologyOuabain-pharmacologyPotassium-bloodRubidium Radioisotopes-bloodSodium-bloodArticlePharmacology