Depolarization produces an acidification of adrenal gland perfusates.
Stimulation of adrenal glands with a variety of agonists or high potassium produced an acidification of the perfusion medium. The magnitude of the transient pH decrease was similar to that found in other nervous structures, and depended on the buffering capacity of the perfusion medium. However, no alkaline transient could be detected in this tissue. This acidification required Ca2+ and occurred under conditions producing catecholamine release. Since firstly the acidification could not be directly correlated with the amount of catecholamine released and secondly the time-course of both phenomena was different, suggesting that the acidification did not only result from the exocytosis of the acidic content of the chromaffin vesicles. The extracellular acidification may in addition originate: (a) partly from the proton release from acidic proteins, (b) from an output of acid equivalents from the cytoplasmic medium, either by the Na+/H+ antiporter present in all animal cells [24], or another mechanism yet to be determined.
Martinez de Munoz
D
D
Unité 338 INSERM, Strasbourg, France.
Burgun
C
C
Aunis
D
D
D000109:Acetylcholine / Q000494:pharmacology; D000110:Acetylcholinesterase / Q000032:analysis*; D000311:Adrenal Glands / Q000378:metabolism*; D000818:Animals; D002021:Buffers; D002118:Calcium / Q000378:metabolism; D002395:Catecholamines / Q000032:analysis*; D002417:Cattle; D002800:Cholinesterase Inhibitors / Q000494:pharmacology; D006863:Hydrogen-Ion Concentration; D007770:L-Lactate Dehydrogenase / Q000032:analysis*; D010477:Perfusion
D002021:Buffers; D002395:Catecholamines; D002800:Cholinesterase Inhibitors; D007770:L-Lactate Dehydrogenase; D000110:Acetylcholinesterase; D000109:Acetylcholine; D002118:Calcium