Characteristics of chloride ion influx in Amphiuma small intestine.
Net Cl- absorption by Amphiuma small intestine is electrogenic but associated with the secretion of HCO3-. To define the mechanisms of Cl- entry into the enterocytes the initial rate of uptake of 36Cl into isolated segments of small intestine was measured. Luminal extracellular space was measured using [3H]inulin. Cl- influx was saturable with a Km of 5.3 mM. When the mucosal medium Cl- concentration was 20 mM influx was linear for 5 min. Cl- influx in 5 min (JiCl) was not reduced by 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid added to the serosal medium, although the Cl- current was abolished. Hence the luminal membrane was the barrier to Cl- uptake. Monovalent anions blocked Cl- influx in the order I- = SCN- = NO3- greater than Br- greater than F-. Anoxia and dinitrophenol reduced JiCl 33 and 71%, respectively. Substitution of medium Na+ with choline or N-methyl glucamine reduced JiCl 60-70%. Removal of medium K+ reduced influx 51%. After medium Na+ and K+ were both replaced influx was stimulated upon reexposure to (Na+ + K+); Na+ alone did not stimulate. JiCl was reduced 34% by furosemide. Neither amiloride nor SITS in the mucosal medium altered influx. JiCl was reduced by replacement of the HCO3- -CO2 buffer with either phosphate or N-2-hydroxyethyl-piperazine-N'-2-ethanesulfonic acid and by exposure to acetazolamide. Theophylline reduced influx 60%, whereas the Ca ionophore A23187 reduced net Cl- absorption and lowered JiCl by 17%. Norepinephrine (10(-5) M) in the serosal bathing medium stimulated Cl- influx 51%. These results indicate that Cl- influx into the intestinal mucosa occurs by a Na+- and, possibly, K+-dependent pathway. Cl- entry is under adrenergic influence.
White
J F
JF
Department of Physiology, Emory University, Atlanta, Georgia 30322.
D000086:Acetazolamide / Q000494:pharmacology; D000818:Animals; D000838:Anions; D001639:Bicarbonates / Q000378:metabolism; D002118:Calcium / Q000502:physiology; D002462:Cell Membrane / Q000378:metabolism; D002712:Chlorides / Q000378:metabolism*; D000242:Cyclic AMP / Q000502:physiology; D005665:Furosemide / Q000494:pharmacology; D007408:Intestinal Absorption / Q000187:drug effects; D007413:Intestinal Mucosa / Q000378:metabolism; D007421:Intestine, Small / Q000378:metabolism*; D007700:Kinetics; D009638:Norepinephrine / Q000494:pharmacology; D011188:Potassium / Q000494:pharmacology; D012964:Sodium / Q000494:pharmacology; D014562:Caudata / Q000378:metabolism*
D000838:Anions; D001639:Bicarbonates; D002712:Chlorides; D005665:Furosemide; D012964:Sodium; D000242:Cyclic AMP; D000086:Acetazolamide; D011188:Potassium; D002118:Calcium; D009638:Norepinephrine