The role of buffer anions and protons in secretion by the rabbit mandibular salivary gland.

Case, R. M.; Conigrave, Arthur D.; Favaloro, Emmanuel J.; Novak, Ivana; Thompson, C.; Young, J. A.

doi:10.1113/jphysiol.1982.sp014037

Cited by 38 publications

(21 citation statements)

References 27 publications

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“…3-6) can most easily be explained by assuming linked ion movements. Na+-Cl-co-transport can be explained either by a combination of Na+-H+ and Cl--HCO3-exchange (Turnberg, Bieberdorf, Morawski & Fordtran, 1970;Case, Conigrave, Favaloro, Novak, Thompson & Young, 1982;Case, Hunter, Novak & Young, 1984) or by Na+-K+2CP-co-transport (Geck, Pietrzyk, Burckhardt, Pfeiffer & Heinz, 1980;Greger & Schlatter, 1981. The crucial discriminatory experiments seem to be the ones investigating the anionic dependence of the ACh-evoked K+ release.…”

Section: Resultsmentioning

confidence: 99%

Acetylcholine‐evoked potassium release in the mouse pancreas.

Petersen¹,

Singh²

1985

The Journal of Physiology

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SUMMARY1. Mouse pancreatic segments were superfused with physiological saline solutions and the K+ concentration in the effluent was measured by flame photometry.2. Acetycholine (ACh) evoked a dose-dependent and transient increase in the K+ concentration in the effluent (K+ release). The removal of calcium (Ca2+) from the superfusing solution and addition of 10-4 M-EGTA (ethyleneglycol-bis-(f-aminoethylether)N,N'-tetraacetic acid) caused a significant reduction in the ACh-elicited K+ outflow.3. Pre-treatment of pancreatic segments with the 'loop diuretics' (furosemide, piretanide and bumetanide; all 10-4 M) resulted in uptake of K+ into the tissue segments. The diuretics also caused a marked reduction in the ACh-induced K+ release.4. Replacement ofchloride (Cl-) in the physiological salt solution by nitrate (NO3), sulphate (SO42-) or iodide (-) caused K+ uptake and a significant reduction in the ACh-evoked K+ release. However, when Cl-was replaced by bromide (Br-) the response to AChf was virtually unaffected.5. When sodium (Na+) was replaced by lithium (Li+) ACh did not evoke K+ release but instead K+ uptake was observed. However, when Tris+ was substituted for Na+ ACh evoked a very small K+ release.6. Pre-treatment of pancreatic segments with 10-3 M-ouabain resulted in a marked sustained K+ release. In the continuing presence of ouabain ACh induced a further increase in K+ outflow. Pre-treatment of the preparation with 10 mM-tetraethylammonium (TEA) caused a small transient increase in K+ efflux, but TEA had virtually no effect on the secretagogue-evoked changes in effluent K+ concentration.7. The results suggest the presence of a diuretic-sensitive Na+-K+Cl-co-transport system in the mouse pancreatic acinar membrane.

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Section: Resultsmentioning

confidence: 99%

Acetylcholine‐evoked potassium release in the mouse pancreas.

Petersen¹,

Singh²

1985

The Journal of Physiology

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“…5 by Eq. 6, we get (7) Where F I /F is the ratio of isosmotic fluorescence to anisosmotic fluorescence. Based on our previous studies on corneal endothelium, we estimate 2 γ to be ~8.…”

Section: Relationship Between Spq Fluorescence Response and Cell Volumementioning

confidence: 99%

Measurement of rapid changes in cell volume by forward light scattering

Srinivas

Bonanno

Larivière

et al. 2003

Pfl�gers Archiv European Journal of Physiology

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The intracellular fluorescence of 6-methoxy-N-(3-sulfopropyl)-quinolinium (SPQ), a Cl − -sensitive fluorescent dye, is quenched by intracellular organic anions and proteins of unknown identity. The concentration of these intracellular quenchers (ICQs), however, is dependent on cell volume. In the absence of Cl − , changes in the observed SPQ fluorescence may therefore reflect changes in cell volume. This concept has been applied to determine relative changes in cell volume of cultured corneal endothelium in response to anisosmotic shocks, using as the Cl − substituent. SPQ fluorescence increased with decreasing osmolarity and vice versa. A 20 mosM hypertonic shock was needed to detect a change in SPQ fluorescence with a signal-to-noise ratio of >25. Assuming dynamic quenching by ICQs, we applied an extension of the Stern-Volmer equation to develop a simple relationship between the measured SPQ fluorescence and relative changes in cell volume. For large hyposmotic shocks, regulatory volume decrease (RVD) was observed. The rate of RVD could be enhanced by exposure to 0.5 μM gramicidin in low-Na+ Ringer solution (i.e., efflux), indicating that K+ conductance is rate limiting for RVD. These results demonstrate the principle of using fluorescence quenching to measure changes in cell volume in real time. Because SPQ is sensitive to Cl − , its usefulness as a quenching probe is limited. However, a structure-activity study can be expected to yield useful Cl − -insensitive analogs.Keywords corneal endothelium; 6-methoxy-N-(3-sulfopropyl)quinolinium; volume regulation Measurement of cell volume, with high temporal resolution and sensitivity, is critical for estimating osmotic water permeability (P f ) (12,14), investigating mechanisms of cell volume regulation (1, 2,9,10,18,23), and ascertaining transient changes in cell volume on stimulation of ion transport mechanisms under isosmotic conditions (11,25). Many techniques to measure cell volume have been developed based on light scattering (11, 12,

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“…This model, originally proposed for the small intestine (Turnberg, Bieberdorf, Morawski & Fordtran, 1970), involves the double exchange of Na+ for H+ and Cl-for HC03- (or OH-). Since some of our preliminary data (Case, Conigrave, Hunter, Novak, Thompson & Young, 1981; were not fully consistent with simple Na+/Cl-co-transport, we contemplated this double counter-exchange system as an alternative model for salivary secretion (Case, Conigrave, Favaloro, Novak, Thompson & Young, 1982).…”

Section: Introductionmentioning

confidence: 99%

The anionic basis of fluid secretion by the rabbit mandibular salivary gland.

Case¹,

Hunter²,

Novak³

et al. 1984

The Journal of Physiology

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SUMMARY1. The role played by anions in salivary secretion has been studied in experiments on the isolated, perfused mandibular gland of the rabbit, in which perfusate Cland/or HCO3-were replaced by other anions.2. Replacement of Cl-with Br-had no significant effect on salivary secretion rate, but replacement with the other anions tested caused secretary rate to fall, by 38 % (I-), 50 % (NO3-)4 61 % (isethionate, ise-), and 66 % (CH3SO4-), respectively.3. Replacement of perfusate Cl-with ise-or CH3SO4-caused the salivary HCO3-concentration to rise up to 4-fold. Replacement with Br-or I-seemed to have little effect on salivary HCO3-concentration but, in contrast to ise-, Br-and I-entered the saliva in concentrations comparable to those of Cl-during control perfusion.4. In glands perfused with HCO3-and ise-, the addition of methazolamide, an inhibitor of carbonic anhydrase, caused a further 60 % drop in secretary rate, but the saliva remained rich in HCO3-. 5. Replacement of perfusate HCO3-with Cl-or ise-had no effect on salivary secretion or composition.6. Replacement of both HCO3-and Cl-in the perfusate with ise-reduced salivary secretion to less than 2 % of control levels.7. In control glands (i.e. perfused with both HC03-and CO-), administration of furosemide, an inhibitor of Na+/Cl-co-transport, reduced the secretion rate and increased salivary HCO3-in a manner indistinguishable from that seen when perfusate Cl-was replaced with ise-.8. In control perfused glands, administration of SITS (4-acetamido-4'-isothiocyano-2,2'-disulphonic acid stilbene), an inhibitor of Cl-/HCO3-antiports, did not cause any change in salivary HCO3-concentration. Unexpectedly, it induced a significant increase in salivary secretary rate. 9. The results show that salivary secretion depends on two independent transport systems. One is a Cl--dependent, furosemide-sensitive system, probably a Na+/Clsymport. The other is an HCO3--dependent, methazolamide-sensitive system, and is probably an Na+/H+ antiport.

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The role of buffer anions and protons in secretion by the rabbit mandibular salivary gland.

Cited by 38 publications

References 27 publications

Acetylcholine‐evoked potassium release in the mouse pancreas.

Acetylcholine‐evoked potassium release in the mouse pancreas.

Measurement of rapid changes in cell volume by forward light scattering

The anionic basis of fluid secretion by the rabbit mandibular salivary gland.

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