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Fritsch, Janine, andAleksander Edelman. of the hyperpolarization-activated chloride in human intestinal T84 cells. Am. J. Physiol. 272 (Cell Physiol. 41): C778-C786, 1997.-The of the hyperpolarization-activated chloride (Iclhyp) in T84 cells was studied using the whole cell patch-clamp recording configuration. Hypotonicity is known to activate an outwardly rectifying chloride (HIORC) distinct from lclhyp in these cells. The differing sensitivities of HIORC and lclhYp toward inhibitors (1,9-dideoxyforskolin blocked HIORC but not IclhYp, and Cd2+ inhibited Iclhyp but not HIORC) allowed us to investigate the osmoregulation of lclhYp. Hypotonicity induced an increase in Iclhyp amplitude. Protein phosphatase inhibitors prevented this effect, and hypotonic solutions became slightly inhibitory. Hypertonicity resulted in a transient increase in Iclhyp amplitude followed by a large decrease. The complex responses of lclhYp to osmotic changes indicate that these signals affect the same channel via multiple transduction pathways. The responses of IclhYp to hypotonicity have features in common with the responses of ClC-2 channels expressed in Xenopus oocytes (activation) and with hyperpolarization-activated chloride s in other cell types, such as osteoblasts and mandibular duct cells (inhibition). volume regulated; ClC-2 CELLS HAVE developed compensatory processes to maintain and restore their volume when exposed to changes in extracellular osmolarity (8,
AJP - Cell Physiology – The American Physiological Society
Published: Mar 1, 1997
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