Okadaic acid inhibits angiotensin II, adrenocorticotropin and potassium-dependent aldosterone secretion.
The present study was designed to assess the effect of okadaic acid (OA), a protein phosphatase inhibitor, on aldosterone secretion in response to angiotensin II (AII), adrenocorticotropin (ACTH) and rises in external potassium concentration (K+). AII (10nM) caused a 20-fold increase in aldosterone production and OA reduced this response by 45%. ACTH (10nM) caused an 8.6-fold increase in aldosterone secretion and OA reduced this by 83%. Increasing K+ concentration from 3 to 12mM caused a 13-fold increase in aldosterone production, which OA inhibited by 36%. These results suggest that protein phosphatases participate in the control of adrenal steroid production, even though ACTH, AII and K+ act via different intracellular messenger systems.
Foster
Richard H
RH
Programa de Fisiología y Biofísica, Instituto de Ciencias Biomédicas, Facultad de Medicina, Universidad de Chile, Casilla 70005, Correo 7, Santiago, Chile. rfoster@machi.med.uchile.cl
Casado
Alín
A
Bakal
Federico
F
Catalán
Lorena
L
Pino
Marcela
M
D000311:Adrenal Glands / Q000166:cytology / Q000378:metabolism; D000324:Adrenocorticotropic Hormone / Q000037:antagonists & inhibitors*; D000450:Aldosterone / Q000378:metabolism*; D000804:Angiotensin II / Q000037:antagonists & inhibitors*; D000818:Animals; D002417:Cattle; D019319:Okadaic Acid / Q000494:pharmacology*; D011188:Potassium / Q000037:antagonists & inhibitors*
D000804:Angiotensin II; D019319:Okadaic Acid; D000450:Aldosterone; D000324:Adrenocorticotropic Hormone; D011188:Potassium