scholarly journals Thyroid hormone regulation of beta-adrenergic receptor number.

1977 ◽  
Vol 252 (8) ◽  
pp. 2787-2789 ◽  
Author(s):  
L T Williams ◽  
R J Lefkowitz ◽  
A M Watanabe ◽  
D R Hathaway ◽  
H R Besch
Endocrinology ◽  
1981 ◽  
Vol 108 (4) ◽  
pp. 1276-1278 ◽  
Author(s):  
PHILIP J. SCARPACE ◽  
ITAMAR B. ABRASS

1994 ◽  
Vol 266 (2) ◽  
pp. L187-L191 ◽  
Author(s):  
M. Nogami ◽  
D. J. Romberger ◽  
S. I. Rennard ◽  
M. L. Toews

Pretreatment of cultured human tracheal smooth muscle cells with transforming growth factor-beta 1 (TGF-beta 1) decreased adenosine 3',5'-cyclic monophosphate (cAMP) accumulation by intact cells stimulated with the beta-adrenergic agonist isoproterenol. The maximal inhibition of isoproterenol-stimulated cAMP accumulation by TGF-beta 1 was 31 +/- 3%, and the mean effective concentration (EC50) of TGF-beta 1 was approximately 1.5 pM. TGF-beta 1 decreased the maximal response to isoproterenol but did not change the EC50 value of isoproterenol. TGF-beta 1 did not change cAMP accumulation stimulated by forskolin. TGF-beta 1 pretreatment decreased isoproterenol-stimulated adenylyl cyclase activity measured in broken cell preparations, but did not change the fluoride-stimulated adenylyl cyclase activity. Together these results suggest that the TGF-beta 1 effect is not by direct inhibition of adenylyl cyclase or by decreased activity of the stimulatory GTP-binding protein. Saturation binding experiments with the beta-adrenergic receptor radioligand [125I]iodopindolol showed that TGF-beta 1 pretreatment decreased the beta-adrenergic receptor number. The protein synthesis inhibitor cycloheximide abolished the effect of TGF-beta 1 on both cAMP accumulation and on beta-adrenergic receptor number, indicating that protein synthesis is involved. These results suggest that TGF-beta 1 in the lung could play a role in changing the responsiveness of airway smooth muscle cells to endogenous catecholamines and to beta-adrenergic agonists used in therapy.


1982 ◽  
Vol 52 (5) ◽  
pp. 1133-1137 ◽  
Author(s):  
R. L. Moore ◽  
M. Riedy ◽  
P. D. Gollnick

Female Sprague-Dawley rats were subjected to endurance-training programs, and the effect of training on myocardial beta-adrenergic receptor number, receptor-binding characteristics, and adenylate cyclase (AC) activities associated with the receptor were examined. Training produced a 45% (P less than 0.01) increase in the succinate dehydrogenase activity of the plantaris muscle. Specific (-)-[3H]dihydroalprenolol (DHA)-binding data were subjected to Scatchard plot analysis to quantify beta-adrenergic receptor number and DHA-binding characteristics of myocardial membranes. The DHA concentrations at which 50% of the total binding sites were occupied were similar for membranes from sedentary (1.95 +/- 0.51) and trained (1.59 +/- 0.34 nM) groups. Total DHA-binding sites of membranes from control (91.6 +/- 13.3) and trained (83.1 +/- 7.6 fmol/mg) groups were also similar. Basal and maximally stimulated AC activities were also unchanged by endurance training. Fluoride-stimulated AC activities of crude homogenate and 10,000 g fractions decreased 47 and 49%, respectively, with training. No differences were observed in a 40,000 g fraction. The specific activities of a ouabain-sensitive Na+-K+-ATPase (a sarcolemmal membrane marker) of crude homogenate, 10,000 g, and 40,000 g membrane fractions were similar. These data indicate that training produces no detectable difference in the potential for adrenergic responses at the receptor level.


1985 ◽  
Vol 5 (5-6) ◽  
pp. 419-429
Author(s):  
William R. Hiatt ◽  
Victoria L. Travis ◽  
Kathryn B. Horwitz ◽  
Lawrence D. Horwitz

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