A critical analysis of carbonic anhydrase function, respiratory gas exchange, and the acid-base control of secretion in the rectal gland of Squalus acanthias. Shuttleworth, T. J., Thompson, J., Munger, R. S., & Wood, C. M. Journal of Experimental Biology, 209(23):4701–4716, December, 2006. doi abstract bibtex We compared in vivo responses of rectal gland secretion to carbonic anhydrase (CA) inhibition (10(-4) mol l(-1) acetazolamide) in volume-loaded dogfish with in vitro responses in an isolated-perfused gland stimulated with 5 10(-6) mol l(-1) forskolin and removed from systemic influences. We also measured respiratory gas exchange in the perfused gland, described the acid-base status of the secreted fluid, and determined the relative importance of various extracellular and intracellular acid-base parameters in controlling rectal gland secretion in vitro. In vivo, acetazolamide inhibited Cl- secretion and decreased pHi in the rectal gland, but interpretation was confounded by an accompanying systemic respiratory acidosis, which would also have contributed to the inhibition. In the perfused gland, M-CO2 and M-O2 increased in linear relation to increases in Cl- secretion rate. CA inhibition (10(-4) mol l(-1) acetazolamide) had no effect on Cl- secretion rate or pHi in the perfused gland, in contrast to in vivo, but caused a transitory 30% inhibition of M-CO2 (relative to stable M-O2) and elevation in secretion P-CO2 effects, which peaked at 2 h and attenuated by 3.5 - 4 h. Secretion was inhibited by acidosis and stimulated by alkalosis; the relationship between relative Cl- secretion rate and pHe was almost identical to that seen in vivo. Experimental manipulations of perfusate pH, P-CO2 and H-CO3 concentration, together with measurements of pHi, demonstrated that these responses were most strongly correlated with changes in pHe, and were not related to changes in P-CO2, extracellular H-CO3(-), or intracellular H-CO3(-) levels, though changes in pHi may also have played a role. The acid-base status of the secreted fluid varied with that of the perfusate, secretion pH remaining about 0.3 - 0.5 units lower, and changing in concert with pHe rather than pHi; secretion H-CO3(-) concentrations remained low, even in the face of greatly elevated perfusate H-CO3(-) concentrations. We conclude that pH effects on rectal gland secretion rate are adaptive, that CA functions to catalyze the hydration of C-O2, thereby maintaining a gradient for diffusive efflux of C-O2 from the working cells, and that differences in response to CA inhibition likely reflect the higher perfusion-to-secretion ratio in vitro than in vivo.
@article{shuttleworth_critical_2006,
title = {A critical analysis of carbonic anhydrase function, respiratory gas exchange, and the acid-base control of secretion in the rectal gland of {Squalus} acanthias},
volume = {209},
shorttitle = {A critical analysis of carbonic anhydrase function, respiratory gas exchange, and the acid-base control of secretion in the rectal gland of {Squalus} acanthias},
doi = {10.1242/jeb.02564},
abstract = {We compared in vivo responses of rectal gland secretion to carbonic anhydrase (CA) inhibition (10(-4) mol l(-1) acetazolamide) in volume-loaded dogfish with in vitro responses in an isolated-perfused gland stimulated with 5 10(-6) mol l(-1) forskolin and removed from systemic influences. We also measured respiratory gas exchange in the perfused gland, described the acid-base status of the secreted fluid, and determined the relative importance of various extracellular and intracellular acid-base parameters in controlling rectal gland secretion in vitro. In vivo, acetazolamide inhibited Cl- secretion and decreased pHi in the rectal gland, but interpretation was confounded by an accompanying systemic respiratory acidosis, which would also have contributed to the inhibition. In the perfused gland, M-CO2 and M-O2 increased in linear relation to increases in Cl- secretion rate. CA inhibition (10(-4) mol l(-1) acetazolamide) had no effect on Cl- secretion rate or pHi in the perfused gland, in contrast to in vivo, but caused a transitory 30\% inhibition of M-CO2 (relative to stable M-O2) and elevation in secretion P-CO2 effects, which peaked at 2 h and attenuated by 3.5 - 4 h. Secretion was inhibited by acidosis and stimulated by alkalosis; the relationship between relative Cl- secretion rate and pHe was almost identical to that seen in vivo. Experimental manipulations of perfusate pH, P-CO2 and H-CO3 concentration, together with measurements of pHi, demonstrated that these responses were most strongly correlated with changes in pHe, and were not related to changes in P-CO2, extracellular H-CO3(-), or intracellular H-CO3(-) levels, though changes in pHi may also have played a role. The acid-base status of the secreted fluid varied with that of the perfusate, secretion pH remaining about 0.3 - 0.5 units lower, and changing in concert with pHe rather than pHi; secretion H-CO3(-) concentrations remained low, even in the face of greatly elevated perfusate H-CO3(-) concentrations. We conclude that pH effects on rectal gland secretion rate are adaptive, that CA functions to catalyze the hydration of C-O2, thereby maintaining a gradient for diffusive efflux of C-O2 from the working cells, and that differences in response to CA inhibition likely reflect the higher perfusion-to-secretion ratio in vitro than in vivo.},
number = {23},
journal = {Journal of Experimental Biology},
author = {Shuttleworth, T. J. and Thompson, J. and Munger, R. S. and Wood, C. M.},
month = dec,
year = {2006},
pages = {4701--4716},
}
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M."],"year":2006,"bibtype":"article","biburl":"http://bibbase.org/zotero/BMSC/","bibdata":{"bibtype":"article","type":"article","title":"A critical analysis of carbonic anhydrase function, respiratory gas exchange, and the acid-base control of secretion in the rectal gland of Squalus acanthias","volume":"209","shorttitle":"A critical analysis of carbonic anhydrase function, respiratory gas exchange, and the acid-base control of secretion in the rectal gland of Squalus acanthias","doi":"10.1242/jeb.02564","abstract":"We compared in vivo responses of rectal gland secretion to carbonic anhydrase (CA) inhibition (10(-4) mol l(-1) acetazolamide) in volume-loaded dogfish with in vitro responses in an isolated-perfused gland stimulated with 5 10(-6) mol l(-1) forskolin and removed from systemic influences. We also measured respiratory gas exchange in the perfused gland, described the acid-base status of the secreted fluid, and determined the relative importance of various extracellular and intracellular acid-base parameters in controlling rectal gland secretion in vitro. In vivo, acetazolamide inhibited Cl- secretion and decreased pHi in the rectal gland, but interpretation was confounded by an accompanying systemic respiratory acidosis, which would also have contributed to the inhibition. In the perfused gland, M-CO2 and M-O2 increased in linear relation to increases in Cl- secretion rate. CA inhibition (10(-4) mol l(-1) acetazolamide) had no effect on Cl- secretion rate or pHi in the perfused gland, in contrast to in vivo, but caused a transitory 30% inhibition of M-CO2 (relative to stable M-O2) and elevation in secretion P-CO2 effects, which peaked at 2 h and attenuated by 3.5 - 4 h. Secretion was inhibited by acidosis and stimulated by alkalosis; the relationship between relative Cl- secretion rate and pHe was almost identical to that seen in vivo. Experimental manipulations of perfusate pH, P-CO2 and H-CO3 concentration, together with measurements of pHi, demonstrated that these responses were most strongly correlated with changes in pHe, and were not related to changes in P-CO2, extracellular H-CO3(-), or intracellular H-CO3(-) levels, though changes in pHi may also have played a role. The acid-base status of the secreted fluid varied with that of the perfusate, secretion pH remaining about 0.3 - 0.5 units lower, and changing in concert with pHe rather than pHi; secretion H-CO3(-) concentrations remained low, even in the face of greatly elevated perfusate H-CO3(-) concentrations. We conclude that pH effects on rectal gland secretion rate are adaptive, that CA functions to catalyze the hydration of C-O2, thereby maintaining a gradient for diffusive efflux of C-O2 from the working cells, and that differences in response to CA inhibition likely reflect the higher perfusion-to-secretion ratio in vitro than in vivo.","number":"23","journal":"Journal of Experimental Biology","author":[{"propositions":[],"lastnames":["Shuttleworth"],"firstnames":["T.","J."],"suffixes":[]},{"propositions":[],"lastnames":["Thompson"],"firstnames":["J."],"suffixes":[]},{"propositions":[],"lastnames":["Munger"],"firstnames":["R.","S."],"suffixes":[]},{"propositions":[],"lastnames":["Wood"],"firstnames":["C.","M."],"suffixes":[]}],"month":"December","year":"2006","pages":"4701–4716","bibtex":"@article{shuttleworth_critical_2006,\n\ttitle = {A critical analysis of carbonic anhydrase function, respiratory gas exchange, and the acid-base control of secretion in the rectal gland of {Squalus} acanthias},\n\tvolume = {209},\n\tshorttitle = {A critical analysis of carbonic anhydrase function, respiratory gas exchange, and the acid-base control of secretion in the rectal gland of {Squalus} acanthias},\n\tdoi = {10.1242/jeb.02564},\n\tabstract = {We compared in vivo responses of rectal gland secretion to carbonic anhydrase (CA) inhibition (10(-4) mol l(-1) acetazolamide) in volume-loaded dogfish with in vitro responses in an isolated-perfused gland stimulated with 5 10(-6) mol l(-1) forskolin and removed from systemic influences. We also measured respiratory gas exchange in the perfused gland, described the acid-base status of the secreted fluid, and determined the relative importance of various extracellular and intracellular acid-base parameters in controlling rectal gland secretion in vitro. In vivo, acetazolamide inhibited Cl- secretion and decreased pHi in the rectal gland, but interpretation was confounded by an accompanying systemic respiratory acidosis, which would also have contributed to the inhibition. In the perfused gland, M-CO2 and M-O2 increased in linear relation to increases in Cl- secretion rate. CA inhibition (10(-4) mol l(-1) acetazolamide) had no effect on Cl- secretion rate or pHi in the perfused gland, in contrast to in vivo, but caused a transitory 30\\% inhibition of M-CO2 (relative to stable M-O2) and elevation in secretion P-CO2 effects, which peaked at 2 h and attenuated by 3.5 - 4 h. 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