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

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The anionic basis of fluid secretion by the rabbit mandibular salivary gland. / Case, R M; Hunter, M; Novak, I; Young, J A.

In: Journal of Physiology, Vol. 349, 1984, p. 619-30.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Case, RM, Hunter, M, Novak, I & Young, JA 1984, 'The anionic basis of fluid secretion by the rabbit mandibular salivary gland.', Journal of Physiology, vol. 349, pp. 619-30.

APA

Case, R. M., Hunter, M., Novak, I., & Young, J. A. (1984). The anionic basis of fluid secretion by the rabbit mandibular salivary gland. Journal of Physiology, 349, 619-30.

Vancouver

Case RM, Hunter M, Novak I, Young JA. The anionic basis of fluid secretion by the rabbit mandibular salivary gland. Journal of Physiology. 1984;349:619-30.

Author

Case, R M ; Hunter, M ; Novak, I ; Young, J A. / The anionic basis of fluid secretion by the rabbit mandibular salivary gland. In: Journal of Physiology. 1984 ; Vol. 349. pp. 619-30.

Bibtex

@article{a018ae20b18d11ddb04f000ea68e967b,
title = "The anionic basis of fluid secretion by the rabbit mandibular salivary gland.",
abstract = "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 Cl- and/or HCO3- were replaced by other anions. Replacement of Cl- with Br- had no significant effect on salivary secretion rate, but replacement with the other anions tested caused secretory rate to fall, by 38% (I-), 50% (NO3-), 61% (isethionate, ise -), and 66% ( CH3SO4 -), respectively. 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. In glands perfused with HCO3- and ise -, the addition of methazolamide, an inhibitor of carbonic anhydrase, caused a further 60% drop in secretory rate, but the saliva remained rich in HCO3-. Replacement of perfusate HCO3- with Cl- or ise - had no effect on salivary secretion or composition. Replacement of both HCO3- and Cl- in the perfusate with ise - reduced salivary secretion to less than 2% of control levels. In control glands (i.e. perfused with both HCO3- and Cl-), 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 -. In control perfused glands, administration of SITS (4-acetamido-4'- isothio cyano-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 secretory rate. The results show that salivary secretion depends on two independent transport systems. One is a Cl- -dependent, furosemide-sensitive system, probably a Na+/Cl- symport. The other is an HCO3- -dependent, methazolamide-sensitive system, and is probably an Na+/H+ antiport.",
author = "Case, {R M} and M Hunter and I Novak and Young, {J A}",
note = "Keywords: 4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid; Animals; Anions; Bicarbonates; Chlorides; Furosemide; Male; Methazolamide; Potassium; Rabbits; Saliva; Secretory Rate; Sodium; Submandibular Gland",
year = "1984",
language = "English",
volume = "349",
pages = "619--30",
journal = "The Journal of Physiology",
issn = "0022-3751",
publisher = "Wiley-Blackwell",

}

RIS

TY - JOUR

T1 - The anionic basis of fluid secretion by the rabbit mandibular salivary gland.

AU - Case, R M

AU - Hunter, M

AU - Novak, I

AU - Young, J A

N1 - Keywords: 4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid; Animals; Anions; Bicarbonates; Chlorides; Furosemide; Male; Methazolamide; Potassium; Rabbits; Saliva; Secretory Rate; Sodium; Submandibular Gland

PY - 1984

Y1 - 1984

N2 - 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 Cl- and/or HCO3- were replaced by other anions. Replacement of Cl- with Br- had no significant effect on salivary secretion rate, but replacement with the other anions tested caused secretory rate to fall, by 38% (I-), 50% (NO3-), 61% (isethionate, ise -), and 66% ( CH3SO4 -), respectively. 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. In glands perfused with HCO3- and ise -, the addition of methazolamide, an inhibitor of carbonic anhydrase, caused a further 60% drop in secretory rate, but the saliva remained rich in HCO3-. Replacement of perfusate HCO3- with Cl- or ise - had no effect on salivary secretion or composition. Replacement of both HCO3- and Cl- in the perfusate with ise - reduced salivary secretion to less than 2% of control levels. In control glands (i.e. perfused with both HCO3- and Cl-), 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 -. In control perfused glands, administration of SITS (4-acetamido-4'- isothio cyano-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 secretory rate. The results show that salivary secretion depends on two independent transport systems. One is a Cl- -dependent, furosemide-sensitive system, probably a Na+/Cl- symport. The other is an HCO3- -dependent, methazolamide-sensitive system, and is probably an Na+/H+ antiport.

AB - 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 Cl- and/or HCO3- were replaced by other anions. Replacement of Cl- with Br- had no significant effect on salivary secretion rate, but replacement with the other anions tested caused secretory rate to fall, by 38% (I-), 50% (NO3-), 61% (isethionate, ise -), and 66% ( CH3SO4 -), respectively. 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. In glands perfused with HCO3- and ise -, the addition of methazolamide, an inhibitor of carbonic anhydrase, caused a further 60% drop in secretory rate, but the saliva remained rich in HCO3-. Replacement of perfusate HCO3- with Cl- or ise - had no effect on salivary secretion or composition. Replacement of both HCO3- and Cl- in the perfusate with ise - reduced salivary secretion to less than 2% of control levels. In control glands (i.e. perfused with both HCO3- and Cl-), 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 -. In control perfused glands, administration of SITS (4-acetamido-4'- isothio cyano-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 secretory rate. The results show that salivary secretion depends on two independent transport systems. One is a Cl- -dependent, furosemide-sensitive system, probably a Na+/Cl- symport. The other is an HCO3- -dependent, methazolamide-sensitive system, and is probably an Na+/H+ antiport.

M3 - Journal article

C2 - 6737303

VL - 349

SP - 619

EP - 630

JO - The Journal of Physiology

JF - The Journal of Physiology

SN - 0022-3751

ER -

ID: 8570548