PMID- 9064643 OWN - NLM STAT- MEDLINE DCOM- 19970314 LR - 20190726 IS - 0031-6768 (Print) IS - 0031-6768 (Linking) VI - 433 IP - 3 DP - 1997 Jan TI - Characterization of swelling-induced ion transport in HT-29Cl.19A cells. Role of inorganic and organic osmolytes during regulatory volume decrease. PG - 276-86 AB - Combined intracellular and transepithelial potential and resistance measurements were performed to localize the ion conductances activated by hypo-osmotic shock of cultured human colonic carcinoma cells (HT-29Cl.19A). Furthermore, the effect of cell swelling induced by a hypo-osmotic solution on the intracellular Ca2+ activity [Ca2+]i and release of amino acids into the extracellular solution was examined. Application of a 40% hypo-osmotic solution on both sides of confluent monolayers induced a hyperpolarization of the intracellular potential caused by increased K+ conductance of the basolateral membrane, followed by a sustained depolarization due to increased Cl- conductance in the apical and basolateral membranes. Usually no transepithelial current occurred, presumably because of random distribution of Cl- channels. However, in some monolayers cell swelling induced a transepithelial Cl- current because of a more pronounced expression of volume-sensitive Cl- channels in the apical membrane. Exposure to hypo-osmotic solution increased [Ca2+]i transiently. The increase of [Ca2+]i was also observed to occur in the presence of the muscarinic receptor agonist carbachol or the inhibitor of the microsomal Ca2+-ATPase thapsigargin (TG), which prevented carbachol-induced Ca2+ release, suggesting that cell swelling recruits Ca2+ from a different source compared to carbachol or TG. Following incubations with hypo-osmotic solutions, about 60% of the intracellular free amino acids including aspartate, glutamate, glycine and taurine was released. It is concluded that the regulatory volume decrease (RVD) in HT-29Cl.19A colonocytes is achieved by activation of K+ and Cl- conductances, resulting in net loss of salt, as well by extrusion of amino acids. FAU - Bajnath, R B AU - Bajnath RB AD - Institute of Neurobiology, Faculty of Biology, University of Amsterdam, Kruislaan 320, NL-1098 SM Amsterdam, The Netherlands. FAU - de Jonge, H R AU - de Jonge HR FAU - Borgdorff, A J AU - Borgdorff AJ FAU - Zuiderwijk, M AU - Zuiderwijk M FAU - Groot, J A AU - Groot JA LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - Germany TA - Pflugers Arch JT - Pflugers Archiv : European journal of physiology JID - 0154720 RN - 0 (Amino Acids) RN - 67526-95-8 (Thapsigargin) SB - IM MH - Amino Acids/metabolism MH - Colon/*drug effects MH - Humans MH - Ion Transport/*drug effects/*physiology MH - Membrane Potentials/*drug effects MH - Thapsigargin/*pharmacology MH - Tumor Cells, Cultured MH - Water-Electrolyte Balance/*drug effects EDAT- 1997/01/01 00:00 MHDA- 1997/01/01 00:01 CRDT- 1997/01/01 00:00 PHST- 1997/01/01 00:00 [pubmed] PHST- 1997/01/01 00:01 [medline] PHST- 1997/01/01 00:00 [entrez] AID - 10.1007/s004240050278 [doi] PST - ppublish SO - Pflugers Arch. 1997 Jan;433(3):276-86. doi: 10.1007/s004240050278.