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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.

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

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.