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The reabsorption of isotonic fluid instilled into the alveolar spaces of anesthesized rabbits has been studied. The role of sodium (Na+) and chlorine (Cl-) ions in this process has been examined by measuring normal saline in the presence or absence of amiloride and in chlorine ion-free solutions. The procedure is repeated after the intratracheal introduction of forskolin which increases cAMP in ATII cells. Results show the transcellular movements of Na+ and Cl- ions regulate the magnitude and direction of fluid fluxes across the alveolar epithelium after cAMP simulation.

The hypothesis that alpha-1- and alpha-2-adrenergic receptors independently regulate lymphocyte amiloride-sensitive sodium channels (ASSC) by utilizing cAMP as a second messenger and by utilizing a GTP-binding protein was investigated. Direct measurements revealed that norepinephrine increased lymphocyte cAMP and activated ASSCs. Terazosin had no effect on the lymphocyte whole cell ASSC currents. This result implied the association between alpha-1-adrenergic receptors to lymphocyte ASSC regulation via GTP-binding proteins.

The molecular weight of the calcium activated chloride channel (CACC) isolated from the trachea of cows is 38 kDa while the predicted molecular weight of the protein transcribed from the postulated coding DNA of CACC is about 100 kDa. A truncated construct of the large protein, CACCX, was expressed in Xenopus eggs to determine if the 38 kDa channel could have been the end product of the posttranslational modification of the 100 kDa peptide. Results indicate that CACCX can function as a chloride channel.

The cystic fibrosis transmembrane conductance regulator (CFTR) was epitope-tagged at its fourth external loop or at its carboxy-terminus with flag epitope (M2) or hemagglutinin A to determine which tag would be useful for studying the targeting of CFTR to its proper location on the plasma membrane. The results show that the M2-tagged CFTR is the most effective tool for studying the trafficking of CFTR to specific locations on the plasma membrane.

Cystic fibrosis (CF) is caused by mutations in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR). A potential animal model of CF, the [CFTR.sup.-/-] mouse, has had limited utility because most mice die from intestinal obstruction during the first month of life. Human CFTR (HCFTR) was expressed in [CFTR.sup.-/-] mice under the control of the rat intestinal fatty acid-binding protein gene promoter. The mice survived and showed functional correction of ileal goblet cell and crypt cell hyperplasia and cyclic adenosine monophosphate-stimulated chloride secretion. These results support the concept that transfer of the HCFTR gene may be a useful strategy for correcting physiologic defects in patients with CF., Cystic fibrosis mice bearing a null mutation in the CFTR gene lack adenosine 3',5'-monophosphate (cAMP)--stimulated [Cl.sup.-] transport in intestinal epithelial cells, which leads to goblet cell hyperplasia, intestinal obstruction, and [...]

Use of Ussing chambers to examine Ca2+ and guanosine 3',5'-cyclic monophosphate (cGMP) modulation of Cl, Na and K transport in isolated porcine distal colon epithelium shows that cGMP activates a bumetanide-sensitive transport pathway to enhance its release while rises in intracellular Ca2+ stimulates multiple anion secretory pathways. HCO3 and bumetanide replacement affect ionomycin-induced Cl- ion release while amiloride has no effect on ionomycin-induced Na absorption. cGMP suppresses the amiloride-inhibited Na+ absorption pathway.

The investigation of the mechanisms of K secretion in the porcine gallbladder epithelium from the neck and the fundus of the organ shows that K is secreted under basal conditions by the porcine gallbladder. The gallbladder was placed in Ussing chambers for investigation after its serosal muscle had been removed. The elevated intracellular calcium concentration, which prohibits the basolateral K effuse, stimulates the K secretion by an additional TEA-insensitive sepical K permeability.

Regional transport characteristics of porcine gallbladder epithelium bathed in Ringer solution in Ussing chamber were studied. Norepinephrine, salbutamol, isoproterenol and dobutamine were administered and their effects on the Na and Cl transport activity observed. Results of the studies confirm regional differences in basal Cl and Na transport. The results also verified alpha2- and beta2-adrenoceptor mediation across the isolated gallbladder epithelium were also noted

Results reveal that the compound SRI 2931 confers sustained and potent activity of transepithelial chloride transport in pancreatic epithelial cells, nasal epithelial cells, and intact tissues from mice used as cystic fibrosis models. The compound increases both ATP and chloride release from apical surfaces of epithelial cells. Further, the calcium transport activation of SRI 2931 show minimal effect on cell proliferation.

Research was conducted to examine the hypothesis that hydrogen peroxide inhibits cAMP-induced Cl- secretion across colonic epithelial cells. Pore-forming antibotics mystatin and amphotericin B were used to permeabilize the basolateral and apical membranes, respectively. Results indicate that H2O2 inhibits Cl-secretion by decreasing the apical plasma membrane Cl-conductance and the activity of the Na+-K+-ATPase.

Presents a study which examined the nitric oxide mechanisms which decreases vectorial Na+ transport across confluent monolayers of rat alveolar type II cells, which were grown on permeable supports. Application of amiloride to the apical side of monolayers; Methodology used to conduct the study; Results of the study.

Elaborates on the inhibition of sodium (Na+) absorption across cultured alveolar type II (ATII) monolayers by nitric oxide (.NO). Decline of Na+ absorption across cultured ATII monolayers with noncytotoxic concentrations of .NO; Inhibition of the amiloride-sensitive Na+ channels.

Describes the synthesis of the calcium (Ca2+)-activated chloride (Cl-) channel (CaCC) and stimulation by phorbol ester. Formation of a functional channel with a smaller form of the CaCC; Regulation of the cloned CaCC by protein kinase C; Two signal transduction systems regulating CaCC isolated from the trachea.