In vitro primate gastric mucosa: electrical characteristics

Abstract

Ion transport by the resting, isolated, rhesus gastric mucosa was assessed under conditions of minimal diffusion limitation to oxygen by 1) the substitution of Na+ and Cl- of the bathing solutions with less permeant ions, 2) the drugs amiloride and ouabain, and 3) estimation of net fluxes of 22Na by methods designed to circumvent the problem of poorly matched tissues. The mucosae developed potential differences of 51.3 +/ 3.5 mV, serosal side positive and had conductances of 5.56 +/- 0.30 mS x cm-2. The permeabilities of the tissues to D-mannitol were between 7.80 x 10(-7) and 3.15 x 10(-7) cm x s-1. The relatively high conductance of this epithelium in the absence of significant edge damage and a low (32%) paracellular conductance stems mainly from a passive permeability to Cl-; active absorption of Na+ and active secretion of Cl- contribute equally to the short-circuit current. The mucosal entry step for Na+ is amiloride sensitive, whereas the serosal exit step can be inhibited by ouabain. The entry step for Cl- at the serosal membrane is possibly sodium dependent.

Role of Na-K-2Cl cotransporter-1 in gastric secretion of nonacidic fluid and pepsinogen

“…7 and 8). The amiloride-sensitive component, now recognized as electrogenic Na ϩ absorption, has been observed in gastric preparations from the rat (15), pig (19), monkey (75), and lizard (31). This absorptive process appears to be a property of mucus-secreting surface epithelial cells that line the corpus and antrum; the strongest evidence for spatial segregation of Na ϩ absorptive and Cl Ϫ secretory functions has come from electrophysiological studies of amphibian (Necturus) gastric mucosa (16).…”

Impedance analysis in epithelia and the problem of gastric acid secretion

“…Microelectrode studies of Necturus gastric mucosa (Spenney, Shoemaker & Sachs, 1974) yielded the estimate that the paracellular pathway contributes only 21% of total transepithelial conductance. 22Na back-flux measurements indicate a contribution of 25% in resting mammalian stomach (Machen, Silen & Forte, 1978;Tripathi & Rangachari, 1980) and even less in stimulated stomach . Both assessments rest on uncertain assumptions.…”

“…The drop in resistance partly accounts for the drop in PD, but the two changes are not directly proportional because short-circuit current I~o also changes. The I~o causing the mucosa-negative PD has two main components: an excess of active C1 -secretion over H § secretion (Hogben 1955;Forte & Machen, 1983); and, in mammals Tripathi & Rangachari, 1980) and reptiles (Hansen, Slegers & Bonting, 1975) but not frogs, active absorption of Na +. Because rates of CI-secretion and Na § absorption vary among species and appear to be influenced to different degrees by histamine stimulation (Machen & Forte, 1979), it is not surprising that the PD response of stimulated gastric mucosa is somewhat variable.…”

“…Finally, Na § absorption by mammal and reptile stomach involves Na + entering the surface cells across the apical membrane by an amiloridesensitive channel and leaving across the basolateral membrane by the Na+/K + ATP-ase Machen & Forte, 1979;Tripathi & Rangachari, 1980). This mechanism appears very similar to the Na § transport mechanism of other tight epithelia such as frog skin (Helman & Fisher, 1977), amphibian urinary bladder (Higgins et al, 1975), and rabbit urinary bladder , with the exception that the possibility of stimulation by aldosterone has not yet been carefully examined for Na + absorption by the stomach.…”