TY - JOUR
T1 - The role of calcium in the induction of refractoriness to cyclic AMP stimulation by TSH
AU - Chayoth, Reuben
AU - Arem, Ridha
AU - Yoshimura, Yoshiyuki
AU - Field, James B.
N1 - Funding Information:
From the Diabetes Research Laboratory, Baylor College of Medicine, Division of Endocrinology and Metabolism, Houston, TX 77030. Supported by United States Public Health Service Grants AM 26088 and AM 27685from the National Institutes of Health. Address reprint requests to Dr James B. Field, Diabetes Research Laboratory, St Luke’s Episcopal Hospital, PO Box 20269. Houston, Texas 77225. 0 I985 by Grune & Stratton, Inc. 0026-0495/85/341220009$03.00/0
PY - 1985/1/1
Y1 - 1985/1/1
N2 - An initial exposure of beef thyroid slices to 25 mU/mL thyroid-stimulating hormone (TSH) for two hours induces a diminished stimulation of cyclic adenosine monophosphate (AMP) production upon subsequent readdition of TSH but does not modify the effect of prostaglandin E1 (PGE1. Incubation of thyroid slices in calcium-free buffer with or without 2 mmol/L ethylene glycol bis (β-aminoethyl ether)-N,N′ = tetracetic acid (EGTA) prevented desensitization induced by TSH and PGE1, to the subsequent stimulation by TSH and PGE1, respectively, despite the presence of calcium in subsequent incubations. TSH-induced desensitization was not modified by increasing the calcium concentration up to 50 mmol/L in the initial incubation. However, the stimulatory effect of TSH upon cyclic AMP levels was decreased as the calcium concentration in the first incubation was increased. In the presence of at least 1 mmol/L calcium, an initial incubation of thyroid slices with 20 μmol/L ionophore A-23187 decreased the stimulation of cyclic AMP by 25 mU/mL TSH added to the slices for the first time during a subsequent incubation. Under these conditions, A-23187 had no effect on PGE1 stimulation of cyclic AMP. These results indicate that calcium may play a role in the TSH-induced, but not PGE1, desensitization of cyclic AMP formation.
AB - An initial exposure of beef thyroid slices to 25 mU/mL thyroid-stimulating hormone (TSH) for two hours induces a diminished stimulation of cyclic adenosine monophosphate (AMP) production upon subsequent readdition of TSH but does not modify the effect of prostaglandin E1 (PGE1. Incubation of thyroid slices in calcium-free buffer with or without 2 mmol/L ethylene glycol bis (β-aminoethyl ether)-N,N′ = tetracetic acid (EGTA) prevented desensitization induced by TSH and PGE1, to the subsequent stimulation by TSH and PGE1, respectively, despite the presence of calcium in subsequent incubations. TSH-induced desensitization was not modified by increasing the calcium concentration up to 50 mmol/L in the initial incubation. However, the stimulatory effect of TSH upon cyclic AMP levels was decreased as the calcium concentration in the first incubation was increased. In the presence of at least 1 mmol/L calcium, an initial incubation of thyroid slices with 20 μmol/L ionophore A-23187 decreased the stimulation of cyclic AMP by 25 mU/mL TSH added to the slices for the first time during a subsequent incubation. Under these conditions, A-23187 had no effect on PGE1 stimulation of cyclic AMP. These results indicate that calcium may play a role in the TSH-induced, but not PGE1, desensitization of cyclic AMP formation.
UR - http://www.scopus.com/inward/record.url?scp=0022387429&partnerID=8YFLogxK
U2 - 10.1016/0026-0495(85)90158-1
DO - 10.1016/0026-0495(85)90158-1
M3 - Article
AN - SCOPUS:0022387429
SN - 0026-0495
VL - 34
SP - 1128
EP - 1132
JO - Metabolism: Clinical and Experimental
JF - Metabolism: Clinical and Experimental
IS - 12
ER -