Potassium ion is indispensable to the catecholamine releasing response of dog adrenals to gamma-aminobutyric acid.
The effect of potassium ion on the GABA-evoked catecholamine (CA) release from isolated perfused adrenal glands of the dog was investigated. When omitting the external potassium ion, the basal release of CA was increased. During this period GABA no longer caused the increase in CA release and moreover the increased basal release was diminished reversibly by GABA. 3-Amino-1-propane-sulfonic acid, a GABAA agonist, mimicked the action of GABA in K+-free solution, while baclofen, a GABAB agonist, did not cause CA release in normal solution and did not alter the basal release in K+-free solution. The inhibition by GABA of the basal CA release in K+-free solution was blocked by bicuculline. The potency of the CA releasing action of GABA was dependent on the concentration of external K+ between 1-10 mM. Reintroduction of K+ to glands which had been perfused with K+-free solution immediately reduced the basal release of CA whereas it recovered the CA releasing action of GABA. These results suggest that GABA-evoked CA release is dependent on potassium ion. The possible mechanisms by which GABA evoked CA release are discussed.
D000311:Adrenal Glands / Q000187:drug effects / Q000378:metabolism*; D000818:Animals; D001640:Bicuculline / Q000494:pharmacology; D002395:Catecholamines / Q000378:metabolism*; D002712:Chlorides / Q000494:pharmacology; D004285:Dogs; D066298:In Vitro Techniques; D011188:Potassium / Q000502:physiology*; D012964:Sodium / Q000494:pharmacology; D013997:Time Factors; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology*
D002395:Catecholamines; D002712:Chlorides; D005680:gamma-Aminobutyric Acid; D012964:Sodium; D011188:Potassium; D001640:Bicuculline