Effect of angiotensin II, ATP, and ionophore A23187 on potassium efflux in adrenal glomerulosa cells.
Angiotensin II stimulus on perifused bovine adrenal glomerulosa cells elicited an increase in 86Rb efflux from cells previously equilibrated with the radioisotope. When 45Ca fluxes were measured under similar conditions, it was observed that Ca and Rb effluxes occurred within the first 30 s of the addition of the hormone and were independent of the presence of external Ca. The 86Rb efflux due to angiotensin II was inhibited by quinine and apamin. The hypothesis that the angiotensin II response is a consequence of an increase in the K permeability of the glomerulosa cell membrane triggered by an increase in cytosolic Ca is supported by the finding that the divalent cation ionophore A23187 also initiated 86Rb or K loss (as measured by an external K electrode). This increased K conductance was also seen with 10(-4) M ATP. Quinine and apamin greatly reduced the effect of ATP or A23187 on 86Rb or K release in adrenal glomerulosa cells. The results suggest that Ca-dependent K channels or carriers are present in the membranes of bovine adrenal glomerulosa cells and are sensitive to hormonal stimulus.
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D000255:Adenosine Triphosphate / Q000494:pharmacology*; D000311:Adrenal Glands / Q000166:cytology / Q000378:metabolism*; D000450:Aldosterone / Q000096:biosynthesis; D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D001030:Apamin / Q000494:pharmacology; D000001:Calcimycin / Q000494:pharmacology*; D002417:Cattle; D011188:Potassium / Q000378:metabolism*; D011803:Quinine / Q000494:pharmacology; D011868:Radioisotopes; D012413:Rubidium / Q000378:metabolism
D011868:Radioisotopes; D000804:Angiotensin II; D001030:Apamin; D000001:Calcimycin; D000450:Aldosterone; D000255:Adenosine Triphosphate; D011803:Quinine; D012413:Rubidium; D011188:Potassium