CO2 hydration in intrapulmonary chemoreceptors

Effects of acetazolamide and benzolamide

T. A. Rodriguez, Steven C Hempleman

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Intrapulmonary chemoreceptors (IPC) are CO2-sensitive sensory neurons that innervate the lungs of birds. Current evidence suggests that IPC CO2 response requires carbonic anhydrase (CA) and that pH is the likely cellular determinant of IPC sensory discharge. In this study we test whether CA enzyme is located intra- or extra-cellularly in IPC by quantifying the effect of relatively membrane permeant lacetazolamide) and relatively impermeant (benzolamide) CA inhibitors on IPC response to CO2. Single fiber recordings were made from 9 anesthetized, unidirectionally ventilated Anas platyrhynchos. Inspired CO2 was stepped from 0% to 7% to identify IPC, and then held steady at levels between 1% and 7% to measure steady IPC response to CO2. Without CA inhibition, IPC discharge rate was inversely proportional to inspired PCO2 (slope -8.9 ± 1.0 sec-1.InTorr-1; μ±sem, n = 9). Infusion of 25 mg/kg benzolamide (i.v.) had no significant effect on IPC CO2 sensitivity (slope -8.5±1.4 sec-1.InTorr-1, n = 7), but 25 mg/kg acetazolamide nearly eliminated sensitivity (slope -0.3 ± 1.0 sec-1.InTorr-1, n = 2). High doses of benzolamide (100 mg/kg) decreased CO2 sensitivity to -3.2 ± 0.6 sec-1.InTorr-1, n = 3, but sensitivity remained greater than with 25mg/kg acetazolamide. Our results suggest that an intracellular rather than extracellular carbonic anhydrase catalyzes hydration of CO2 to carbonic acid in IPC, and that intracellular H+ controls IPC discharge rate.

Original languageEnglish (US)
JournalFASEB Journal
Volume11
Issue number3
StatePublished - 1997

Fingerprint

Benzolamide
acetazolamide
Acetazolamide
Carbonic Anhydrases
chemoreceptors
Hydration
carbonate dehydratase
Carbonic Acid
Carbonic Anhydrase Inhibitors
Birds
Sensory Receptor Cells
Neurons
Membranes
Lung
Fibers
Enzymes
carbonic acid
sensory neurons
Anas platyrhynchos

ASJC Scopus subject areas

  • Agricultural and Biological Sciences (miscellaneous)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Biochemistry
  • Cell Biology

Cite this

CO2 hydration in intrapulmonary chemoreceptors : Effects of acetazolamide and benzolamide. / Rodriguez, T. A.; Hempleman, Steven C.

In: FASEB Journal, Vol. 11, No. 3, 1997.

Research output: Contribution to journalArticle

@article{e0b64ae0c2e84e8783f09e5018947cea,
title = "CO2 hydration in intrapulmonary chemoreceptors: Effects of acetazolamide and benzolamide",
abstract = "Intrapulmonary chemoreceptors (IPC) are CO2-sensitive sensory neurons that innervate the lungs of birds. Current evidence suggests that IPC CO2 response requires carbonic anhydrase (CA) and that pH is the likely cellular determinant of IPC sensory discharge. In this study we test whether CA enzyme is located intra- or extra-cellularly in IPC by quantifying the effect of relatively membrane permeant lacetazolamide) and relatively impermeant (benzolamide) CA inhibitors on IPC response to CO2. Single fiber recordings were made from 9 anesthetized, unidirectionally ventilated Anas platyrhynchos. Inspired CO2 was stepped from 0{\%} to 7{\%} to identify IPC, and then held steady at levels between 1{\%} and 7{\%} to measure steady IPC response to CO2. Without CA inhibition, IPC discharge rate was inversely proportional to inspired PCO2 (slope -8.9 ± 1.0 sec-1.InTorr-1; μ±sem, n = 9). Infusion of 25 mg/kg benzolamide (i.v.) had no significant effect on IPC CO2 sensitivity (slope -8.5±1.4 sec-1.InTorr-1, n = 7), but 25 mg/kg acetazolamide nearly eliminated sensitivity (slope -0.3 ± 1.0 sec-1.InTorr-1, n = 2). High doses of benzolamide (100 mg/kg) decreased CO2 sensitivity to -3.2 ± 0.6 sec-1.InTorr-1, n = 3, but sensitivity remained greater than with 25mg/kg acetazolamide. Our results suggest that an intracellular rather than extracellular carbonic anhydrase catalyzes hydration of CO2 to carbonic acid in IPC, and that intracellular H+ controls IPC discharge rate.",
author = "Rodriguez, {T. A.} and Hempleman, {Steven C}",
year = "1997",
language = "English (US)",
volume = "11",
journal = "FASEB Journal",
issn = "0892-6638",
publisher = "FASEB",
number = "3",

}

TY - JOUR

T1 - CO2 hydration in intrapulmonary chemoreceptors

T2 - Effects of acetazolamide and benzolamide

AU - Rodriguez, T. A.

AU - Hempleman, Steven C

PY - 1997

Y1 - 1997

N2 - Intrapulmonary chemoreceptors (IPC) are CO2-sensitive sensory neurons that innervate the lungs of birds. Current evidence suggests that IPC CO2 response requires carbonic anhydrase (CA) and that pH is the likely cellular determinant of IPC sensory discharge. In this study we test whether CA enzyme is located intra- or extra-cellularly in IPC by quantifying the effect of relatively membrane permeant lacetazolamide) and relatively impermeant (benzolamide) CA inhibitors on IPC response to CO2. Single fiber recordings were made from 9 anesthetized, unidirectionally ventilated Anas platyrhynchos. Inspired CO2 was stepped from 0% to 7% to identify IPC, and then held steady at levels between 1% and 7% to measure steady IPC response to CO2. Without CA inhibition, IPC discharge rate was inversely proportional to inspired PCO2 (slope -8.9 ± 1.0 sec-1.InTorr-1; μ±sem, n = 9). Infusion of 25 mg/kg benzolamide (i.v.) had no significant effect on IPC CO2 sensitivity (slope -8.5±1.4 sec-1.InTorr-1, n = 7), but 25 mg/kg acetazolamide nearly eliminated sensitivity (slope -0.3 ± 1.0 sec-1.InTorr-1, n = 2). High doses of benzolamide (100 mg/kg) decreased CO2 sensitivity to -3.2 ± 0.6 sec-1.InTorr-1, n = 3, but sensitivity remained greater than with 25mg/kg acetazolamide. Our results suggest that an intracellular rather than extracellular carbonic anhydrase catalyzes hydration of CO2 to carbonic acid in IPC, and that intracellular H+ controls IPC discharge rate.

AB - Intrapulmonary chemoreceptors (IPC) are CO2-sensitive sensory neurons that innervate the lungs of birds. Current evidence suggests that IPC CO2 response requires carbonic anhydrase (CA) and that pH is the likely cellular determinant of IPC sensory discharge. In this study we test whether CA enzyme is located intra- or extra-cellularly in IPC by quantifying the effect of relatively membrane permeant lacetazolamide) and relatively impermeant (benzolamide) CA inhibitors on IPC response to CO2. Single fiber recordings were made from 9 anesthetized, unidirectionally ventilated Anas platyrhynchos. Inspired CO2 was stepped from 0% to 7% to identify IPC, and then held steady at levels between 1% and 7% to measure steady IPC response to CO2. Without CA inhibition, IPC discharge rate was inversely proportional to inspired PCO2 (slope -8.9 ± 1.0 sec-1.InTorr-1; μ±sem, n = 9). Infusion of 25 mg/kg benzolamide (i.v.) had no significant effect on IPC CO2 sensitivity (slope -8.5±1.4 sec-1.InTorr-1, n = 7), but 25 mg/kg acetazolamide nearly eliminated sensitivity (slope -0.3 ± 1.0 sec-1.InTorr-1, n = 2). High doses of benzolamide (100 mg/kg) decreased CO2 sensitivity to -3.2 ± 0.6 sec-1.InTorr-1, n = 3, but sensitivity remained greater than with 25mg/kg acetazolamide. Our results suggest that an intracellular rather than extracellular carbonic anhydrase catalyzes hydration of CO2 to carbonic acid in IPC, and that intracellular H+ controls IPC discharge rate.

UR - http://www.scopus.com/inward/record.url?scp=26344435755&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=26344435755&partnerID=8YFLogxK

M3 - Article

VL - 11

JO - FASEB Journal

JF - FASEB Journal

SN - 0892-6638

IS - 3

ER -