Ion transport in dog tracheal mucosa: interaction between calcium and prostaglandins

Publisher Website
Google Scholar
Abstract
Prostaglandin [PG] E1 and PGF2.alpha. stimulate short-circuit current (SCC), tissue conductance (G), and net Cl secretion by canine tracheal mucosa. To determine if these actions of PG require extracellular Ca the effects of PGE1 and PGF2.alpha. on tracheal mucosa mounted in Ussing chambers were tested when 1 side of the preparation was exposed to 0.2 mM ethyleneglycol-bis(.beta.-aminoethylether)-N,N,N'',N''-tetraacetic acid in Krebs-Henseleit solution without Ca. Lack of Ca from the mucosal bath was associated with increased G, lowered potential difference (PD), and severalfold increase of 22Na and 36Cl fluxes in both directions. Addition of 1 .mu.M of PGE1 or PGF2.alpha. to the Ca-free mucosal bath raised PD by 6 mV and SCC by 15 .mu.A .cntdot. cm-2 but decreased G by 1.4 mS .cntdot. cm-2. Unidirectional 22Na and 36Cl fluxes decreased by 32-49% (n = 7, P < 0.05). The increase in G, most likely of the paracellular pathway and brought about by the lack of mucosal Ca, apparently was partially reversible by PGE1 and PGF2.alpha.. When tissues were exposed to Ca-free solution on their submucosal side, PGE1 or PGF2.alpha. were not able to reverse the progressive decline in PD and tissue resistance (n = 8). [14C]mannitol flux increased when Ca was absent from the mucosal bath; then addition of 1 .mu.M PGF2.alpha. caused a 37% decline in flux (n = 5). The increase in the flux of [14C]mannitol found when the submucosal bath lacked Ca was not reversed by 1 .mu.M PGE1. PGE1 and PGF2.alpha. stimulate SCC when added to the bath lacking Ca, indicating that their effect on SCC is not crucially dependent on extracellular Ca. PG decrease the G of the paracellular pathways that were altered by the selective lack of luminal Ca, suggesting that while PG increase cellular conductance they can concurrently decrease paracellular conductance. The latter effect might involve structural alterations of tight junctions or mobilization of Ca onto the Ca-depleted intercellular structures.

This publication has 1 reference indexed in Scilit: