The location of carbonic anhydrase in relation to the blood-brain barrier at the medullary chemoreceptors of the cat.

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Abstract
The role of carbonic anhydrase near the medullary chemoreceptors was investigated in the cat. Vertebral artery injections were used to cause abrupt changes in respiration as a result of changes in the activity of medullary chemoreceptors. Injections of 100% CO2-saline were used to stimulate respiration and of Tris or alkalinized albumin solution to cause a reduction in respiration. The injections gave rapid effects. The effect of benzolamide (1-4 mg/kg i.v.), a carbonic anhydrase inhibitor which does not easily cross the blood-brain barrier, and acetazolamide (50 mg/kg i.v.), an inhibitor which crosses the barrier more easily, were studied. Effects of Tris were much reduced after benzolamide. Even addition of benzolamide to the injected Tris or ablumin was sufficient to reduce their effects. Effects of CO2-saline were reduced only after acetazolamide i.v. Whereas addition of carbonic anhydrase to injected Tris potentiated the effects on respiration, after acetazolamide this potentiation was much less marked. Carbonic anhydrase apparently acts in the region of the medullary chemoreceptors at 2 sites: outside the blood-brain barrier, probably at the luminal surface of the capillary endothelium, where it may act on plasma buffers, and inside the barrier, in association with the chemoreceptors, where it may accelerate CO2/pH equilibration.