Potentiometric determination of carbonic anhydrase activity in rabbit carotid bodies: Comparison among normoxic, hyperoxic and hypoxic animals

Botrè, Francesco; Botrê, Claudio; Greco, Anita; Data, P. G.; Giulio, Camillo Di; Morelli, Luca

doi:10.1016/0304-3940(94)90467-7

Cited by 9 publications

(8 citation statements)

References 13 publications

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“…Whilst this may also have been, at least in part, an effect of acetazolamide upon maxiK channels (700), there has been no indication of such CO 2 -O 2 interaction occurring at the level of maxiK channels in type I cells (691), although a potentiating effect of hypercapnia upon hypoxia has been noted at the level of Ca 2+ signaling (184). The effect of acetazolamide on CO 2 -O 2 interaction in the reflex studies of Teppema and colleagues was less in hyperoxia than hypoxia, which may reflect a functional consequence of the O 2 sensitivity of carotid body carbonic anhydrase (97). …”

Section: Other Physiological Stimuli Of the Carotid Bodymentioning

confidence: 91%

Peripheral Chemoreceptors: Function and Plasticity of the Carotid Body

Kumar

Prabhakar

2012

Comprehensive Physiology

460

572

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The discovery of the sensory nature of the carotid body dates back to the beginning of the 20th century. Following these seminal discoveries, research into carotid body mechanisms moved forward progressively through the 20th century, with many descriptions of the ultrastructure of the organ and stimulus-response measurements at the level of the whole organ. The later part of 20th century witnessed the first descriptions of the cellular responses and electrophysiology of isolated and cultured type I and type II cells, and there now exist a number of testable hypotheses of chemotransduction. The goal of this article is to provide a comprehensive review of current concepts on sensory transduction and transmission of the hypoxic stimulus at the carotid body with an emphasis on integrating cellular mechanisms with the whole organ responses and highlighting the gaps or discrepancies in our knowledge. It is increasingly evident that in addition to hypoxia, the carotid body responds to a wide variety of blood-borne stimuli, including reduced glucose and immune-related cytokines and we therefore also consider the evidence for a polymodal function of the carotid body and its implications. It is clear that the sensory function of the carotid body exhibits considerable plasticity in response to the chronic perturbations in environmental O2 that is associated with many physiological and pathological conditions. The mechanisms and consequences of carotid body plasticity in health and disease are discussed in the final sections of this article.

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Section: Other Physiological Stimuli Of the Carotid Bodymentioning

confidence: 91%

Peripheral Chemoreceptors: Function and Plasticity of the Carotid Body

Kumar

Prabhakar

2012

Comprehensive Physiology

460

572

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“…Type I cells contain CA isoenzymes of which the precise subcellular locations remain to be elucidated except for the cytosolic isoforms CA II and III (possibly a membrane‐bound isoform is also involved Rigual et al 1985; Nurse, 1990; Botrè et al 1994; Ridderstråle & Hanson, 1984; Yamamoto et al 2003). There are ample data to indicate that in the carotid bodies, CA regulates the speed and magnitude of changes in intracellular pH of type I cells upon (removal of) sudden hypercapnic stimuli (Gray, 1971; Black et al .…”

Section: Discussionmentioning

confidence: 99%

The carbonic anhydrase inhibitors methazolamide and acetazolamide have different effects on the hypoxic ventilatory response in the anaesthetized cat

Teppema¹,

Bijl²,

Gourabi³

et al. 2006

The Journal of Physiology

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We compared the effects of the carbonic anhydrase inhibitors methazolamide and acetazolamide (3 mg kg -1 , I.V.) on the steady-state hypoxic ventilatory response in 10 anaesthetized cats. In five additional animals, we studied the effect of 3 and 33 mg kg -1 methazolamide. The steady-state hypoxic ventilatory response was described by the exponential function:whereV I is the inspired ventilation , G is hypoxic sensitivity, D is the shape factor and A is hyperoxic ventilation. In the first group of 10 animals, methazolamide did not change parameters G and D, while A increased from 0.86 ± 0.33 to 1.30 ± 0.40 l min -1 (mean ± S.D., P = 0.003). However, the subsequent administration of acetazolamide reduced G by 44% (control, 1.93 ± 1.32; acetazolamide, 1.09 ± 0.92 l min -1 , P = 0.003), while A did not show a further change. Acetazolamide tended to reduce D (control, 0.20 ± 0.07; acetazolamide, 0.14 ± 0.06 kPa -1 , P = 0.023). In the second group of five animals, neither low-nor high-dose methazolamide changed parameters G, D and A. The observation that even high-dose methazolamide, causing full inhibition of carbonic anhydrase in all body tissues, did not reduce the hypoxic ventilatory response is reminiscent of previous findings by others showing no change in magnitude of the hypoxic response of the in vitro carotid body by this agent. This suggests that normal carbonic anhydrase activity is not necessary for a normal hypoxic ventilatory response to occur. The mechanism by which acetazolamide reduces the hypoxic ventilatory response needs further study.

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“…The peripheral and central chemoreceptors contain CA [23,24], although it is not known which isozymes (intracellular or plasma membrane bound) are present. Inhibition of chemoreceptor CA also contributes to the overall effect of CA inhibitors on breathing but, in contrast to the stimulant systemic acid-base effects described above, depressant effects are often observed in the absence of red cell and renal CA inhibition.…”

Section: Ventilatory Effects Of Ca Inhibitorsmentioning

confidence: 99%