Intraepithelial current flow in rat pancreatic secretory epithelia

Evans, Luke; Pirani, D.; Cook, David I.; Young, J. A.

doi:10.1007/bf00584938

Cited by 26 publications

(8 citation statements)

References 25 publications

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“…Thus, secretin-stimulated fluid transport should be reduced if the basolateral K+ channels are blocked, and this is exactly what we found when ducts were exposed to barium or TEA. Previously, it has been reported that these blockers (at the same concentrations we have employed) have no effect on fluid transport from the perfused rat pancreas stimulated with secretin, at least over a 10 min exposure period (Evans, Pirani, Cook & Young, 1986). It is possible that during our longer, 1 h exposure time, TEA and barium have toxic effects on the duct cells.…”

Section: Discussionmentioning

confidence: 80%

Characteristics of fluid secretion from isolated rat pancreatic ducts stimulated with secretin and bombesin.

Ashton¹,

Argent²,

Green³

1991

The Journal of Physiology

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SUMMARY1. Micropuncture techniques were used to study the cellular mechanisms of fluid secretion by interlobular ducts isolated from the pancreas of copper-deficient rats.2. Perifusing ducts with a calcium-free buffer containing 5 mM-EGTA reduced the volume of fluid secreted in the presence of 10 nM-bombesin by 62 %, whereas fluid secretion measured in the presence of 10 nM-secretin was reduced by only 26 %. 4. SITS (4-acetamido-4'-isothiocyanatostilbene-2,2'-disulphonic acid; mM), reduced fluid secretion measured in the presence of bombesin by 61 %, but had no effect on the response to secretin. 5. The K+ channel blockers, barium (3 mM) and tetraethylammonium (TEA; 10 mM), inhibited fluid secretion measured in the presence of both secretin and bombesin by between 52 and 66%.6. From these results, we conclude that secretin and bombesin may utilize different intracellular signalling pathways and, furthermore, may activate different anion secretory mechanisms within the pancreatic ductal epithelium. However, the effect of the potassium channel blockers is consistent with both peptides activating secretory mechanisms which are electrogenic, and which depend for their operation on potassium efflux across the basolateral membrane of the duct cell.

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Section: Discussionmentioning

confidence: 80%

Characteristics of fluid secretion from isolated rat pancreatic ducts stimulated with secretin and bombesin.

Ashton¹,

Argent²,

Green³

1991

The Journal of Physiology

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“…During perfusion with Ba2+ alone flow rate was rapidly and almost completely inhibited in contrast to the results shown in this figure. We interpret this inhibition as a side-effect of the increase in intraglandular pressure (but see Evans, Pirani, Cook & Young, 1986). 1 /M-verapamil alone had no effect on flow rate or electrolyte composition.…”

Section: The Effects Of Bariummentioning

confidence: 99%

The effects of bumetanide, amiloride and Ba2+ on fluid and electrolyte secretion in rabbit salivary gland.

Lau

Howorth

Case

1990

The Journal of Physiology

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SUMMARY1. In order to distinguish between models of anion secretion, the effects of transport inhibitors on saliva flow rate and electrolyte composition were studied during the plateau phase of secretion in rabbit mandibular salivary glands.2. Bumetanide, an inhibitor of Na+,K+,2CP-co-transport, inhibited flow rate (by 60%) and reduced Cl-concentration. K+ and HC03-concentrations were increased. Forskolin, an adenylate cyclase activator which inhibits ductal transport, did not significantly affect this pattern of changes.3. Amiloride, used at concentrations that would inhibit Na+-H+ exchange, inhibited flow rate (by 30 %). Cl-concentration was initially increased before subsequently decreasing at the same time as HC03-concentration increased. These concentration changes can probably be attributed to ductal transport. When amiloride was applied to glands perfused with nominally HCO3--free solutions, inhibition of flow rate was rapid and almost complete.4. When amiloride and bumetanide were both present in the perfusate, flow rate was inhibited by 92%. The pattern of electrolyte changes was not significantly different from that observed in the presence of bumetanide alone.5. Inhibition of K+ channel activity using Ba2+ also inhibited flow rate. Cl--concentration was increased as was K+ concentration. HC03-concentration was not increased.6. The anion exchange inhibitor DIDS (4,4'-diisothiocyanatostilbene-2,2'-disulphonic acid) had no effect on either flow rate or electrolyte concentration. It did, however, elicit secretion in the absence of acetylcholine.7. The data suggest that Na+-H+ and Cl--HCO3-exchangers are unlikely to be involved in fluid and electrolyte secretion in these glands as suggested by some authors. Most of the data can be explained by postulating the existence of nonspecific anion channels in the apical membranes of the acinar cells.

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“…Such an effect would explain the dosedependent increase in pancreatic juice K + concentration (from 5 to 10 raM) that has been shown to occur following stimulation of the rat pancreas with secretin [33]. Although it has been reported that Ba 2+ has no effect on secretin-stimulated fluid secretion from the perfused rat pancreas [9], this could be explained by poor uptake of Ba 2 § into the duct cell since it is thought to block the channel from the inside face of the plasma membrane [39].…”

Section: Discussionmentioning

confidence: 94%

Regulation of maxi-K+ channels on pancreatic duct cells by cyclic AMP-dependent phosphorylation

Gray¹,

Greenwell²,

Garton³

et al. 1990

J. Membrain Biol.

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Using the patch-clamp technique we have identified a Ca2(+)-sensitive, voltage-dependent, maxi-K+ channel on the basolateral surface of rat pancreatic duct cells. The channel had a conductance of approximately 200 pS in excised patches bathed in symmetrical 150 mM K+, and was blocked by 1 mM Ba2+. Channel open-state probability (Po) on unstimulated cells was very low, but was markedly increased by exposing the cells to secretin, dibutyryl cyclic AMP, forskolin or isobutylmethylxanthine. Stimulation also shifted the Po/voltage relationship towards hyperpolarizing potentials, but channel conductance was unchanged. If patches were excised from stimulated cells into the inside-out configuration, Po remained high, and was not markedly reduced by lowering bath (cytoplasmic) Ca2+ concentration from 2 mM to 0.1 microM. However, activated channels were still blocked by 1 mM Ba2+. Channel Po was also increased by exposing the cytoplasmic face of excised patches to the purified catalytic subunit of cyclic AMP-dependent protein kinase. We conclude that cyclic AMP-dependent phosphorylation can activate maxi-K+ channels on pancreatic duct cells via a stable modification of the channel protein itself, or a closely associated regulatory subunit, and that phosphorylation alters the responsiveness of the channels to Ca2+. Physiologically, these K+ channels may contribute to the basolateral K+ conductance of the duct cell and, by providing a pathway for current flow across the basolateral membrane, play an important role in pancreatic bicarbonate secretion.

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Intraepithelial current flow in rat pancreatic secretory epithelia

Cited by 26 publications

References 25 publications

Characteristics of fluid secretion from isolated rat pancreatic ducts stimulated with secretin and bombesin.

Characteristics of fluid secretion from isolated rat pancreatic ducts stimulated with secretin and bombesin.

The effects of bumetanide, amiloride and Ba2+ on fluid and electrolyte secretion in rabbit salivary gland.

Regulation of maxi-K+ channels on pancreatic duct cells by cyclic AMP-dependent phosphorylation

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