Beta-adrenergic modulation of mucin secretion in cat trachea

1983 ◽  
Vol 244 (5) ◽  
pp. C391-C398 ◽  
Author(s):  
C. M. Liedtke ◽  
S. A. Rudolph ◽  
T. F. Boat
Keyword(s):  
Protein Kinases ◽  
Type Ii ◽  
Adrenergic Agonists ◽  
Mucin Secretion ◽  
Beta Adrenergic ◽  
Beta Adrenergic Agonists ◽  
Adrenergic Modulation ◽  
Dependent Protein ◽  
Mucin Release ◽  
Camp Levels

The mechanism of beta-adrenergic regulation of mucin secretion was investigated in cat trachea in vitro. beta-Adrenergic agonists increased the release of [35S]SO4-radiolabeled mucin and mucosa-submucosal adenosine 3',5'-cyclic monophosphate (cAMP) levels in a dose- and time-dependent manner. The relative potencies and efficacies of l-isoproterenol, l-epinephrine, l-norepinephrine, terbutaline, and dobutamine for physiological and biochemical events were similar. The effect of these agonists were blocked by d-l-propranolol. 3-Isobutyl-l-methylxanthine (IBMX) and 8-bromo-cAMP mimicked the effects of the agonists on mucin release. IBMX increased cAMP levels and potentiated the increase in cAMP levels effected by beta-adrenergic agonists. The half-maximal effects of l-isoproterenol on cAMP levels and mucin release were attained at 1.6 and 8.8 min, respectively. Three major mucosa-submucosal proteins of apparent molecular weights of 49,000, 54,000, and 59,000 daltons displayed reduced binding of the photoaffinity label 8-N3-[32P]cAMP when endogenous cAMP levels were increased with l-isoproterenol and/or IBMX. The first two proteins correspond in electrophoretic mobility to the regulatory subunits of type I and type II cAMP-dependent protein kinases, respectively. The 59,000-dalton cAMP binding protein may be the phosphorylated form of the regulatory subunit of type II cAMP-dependent protein kinase. These data are consistent with the hypothesis that beta-adrenergic modulation of tracheal mucin release is mediated by cAMP and suggest that activation of cAMP-dependent protein kinases may be involved in the neurohormonal effects.

Physiological responsiveness of isolated rabbit tracheal epithelial cells

1984 ◽  
Vol 247 (5) ◽  
pp. C441-C449 ◽  
Author(s):  
C. M. Liedtke ◽  
B. Tandler
Keyword(s):  
Epithelial Cells ◽  
Binding Proteins ◽  
Dependent Manner ◽  
Adrenergic Agonists ◽  
Intact Cells ◽  
Beta Adrenergic ◽  
Tracheal Epithelial Cells ◽  
Beta Adrenergic Agonists ◽  
Tracheal Epithelial ◽  
Camp Levels

Surface tracheal epithelial cells (tracheocytes) from rabbit were isolated by treating intact tissue with chelators and proteolytic enzymes. The cells were viable as assessed by the following criteria: fluorescent viability staining, sequestration of lactate dehydrogenase, and maintenance of constant ATP levels. Radiolabeled Na+ was transported into cells with a rate constant of 0.06/min and an initial velocity of 1.6 nmol X 10(6) cells-1 X min-1 X beta-adrenergic agonists increased adenosine 3',5'-cyclic monophosphate (cAMP) levels in a time- and dose-dependent manner. The beta-adrenergic effects were potentiated by the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine and blocked by propranolol. The tracheocytes retained the capacity to respond to beta-adrenergic agonists for at least 90 min after isolation. Two major cAMP binding proteins of apparent molecular weights of 50,000 and 54,000 were identified in tracheocytes with the photoaffinity label 8-N3-[32P]cAMP. Agents that increased cAMP levels in intact cells and unlabelled cAMP added to homogenates of cells that were not exposed to drugs decreased photoaffinity labeling. The two proteins correspond in electrophoretic mobility to the regulatory subunits of cAMP-dependent protein kinases I and II, respectively. The results demonstrate that the beta-adrenergic receptors and cAMP binding proteins identified in rabbit tracheal mucosa submucosa are present on tracheocytes, suggesting a role for these receptors in the regulation of tracheocyte physiological events.

Sodium-independent modulation of Na(+)-K(+)-ATPase activity by beta-adrenergic agonist in alveolar type II cells

1995 ◽  
Vol 268 (6) ◽  
pp. L983-L990 ◽  
Author(s):  
S. Suzuki ◽  
D. Zuege ◽  
Y. Berthiaume
Keyword(s):  
Atpase Activity ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Adrenergic Agonists ◽  
Adrenergic Agonist ◽  
Alveolar Type Ii Cells ◽  
Beta Adrenergic ◽  
Beta Adrenergic Agonists ◽  
Beta Adrenergic Agonist

Although beta-adrenergic agonists are known to stimulate sodium transport in alveolar epithelial cells, the exact cellular mechanism involved in this process is unknown. We determined whether terbutaline, a beta-adrenergic agonist, modulated Na(+)-K(+)-ATPase in cultured rat alveolar type II cells by measuring the enzyme's activity via an adapted radiometric method. The assay conditions were optimized by evaluating permeabilization techniques and substrate concentrations for Na(+)-K(+)-ATPase measurement at maximum velocity enzyme reaction (Vmax). Terbutaline at 10(-2) M increased enzyme activity, with a maximal response at 15 min that was completely inhibited by 10(-2) M propranolol. This effect of terbutaline was dependent on the presence of serum as well as on the time the cells were in culture. The enhancement of Na(+)-K(+)-ATPase activity was reproduced by 10(-3) M dibutyryl adenosine 3',5'-cyclic monophosphate and 5 x 10(-5) M forskolin. Neither 10(-4) M amiloride nor a sodium-free solution influenced the effect of terbutaline. Western blotting showed that terbutaline did not change the expression of the alpha 1-subunit of the enzyme, which is the predominant form in this cell type. We conclude that beta-adrenergic agonists can modulate Na(+)-K(+)-ATPase activity partially through adenosine 3',5'-cyclic monophosphate and this process is not secondary to an increase in intracellular sodium concentration.w

Sympathetic nervous system and renin release from submaxillary glands in vitro

1976 ◽  
Vol 231 (2) ◽  
pp. 551-554 ◽  
Author(s):  
AM Michelakis ◽  
JW Menzie ◽  
H Yoshida
Keyword(s):  
Direct Action ◽  
Submaxillary Gland ◽  
Renin Release ◽  
Adrenergic Agonists ◽  
Beta Adrenergic ◽  
Submaxillary Glands ◽  
Beta Adrenergic Agonists ◽  
Camp Levels

We previously reported that alpha- but not beta-adrenergic agonists stimulate renin release from mouse submaxillary glands in vivo. The present studies were undertaken to determine if these in vivo effects were due to a direct action on the submaxillary glands and to find out if cyclic AMP (cAMP) might be involved in submaxillary renin release. Pooled mouse submaxillary gland slices were incubated in Krebs-Ringer bicarbonate medium following a preincubation period, and renin release was measured by a radioimmunoassay for the direct measurement of submaxillary gland renin. Tissue cAMP levels were also measured. Addition of the alpha-adrenergic agonists, phenylephrine or norepinephrine, significantly increased renin release (P less than 0.01 vs. control) while decreasing tissue cAMP levels (P less than 0.01 vs. control). In contrast, addition of the beta-adrenergic agonist isoproterenol markedly increased cAMP levels (P less than 0.01 vs. control) and decreased renin release (P less than 0.05 vs. control). Pretreatment of the slices with the alpha-blocker phenoxy genzamine inhibited the effect of phenylephrine. These results indicate that alpha-adrenergic agonists cause renin release from submaxillary glands which is accompanied by a fall in tissue cAMP levels. This is in contrast to renin release from the kidney which is stimulated by beta-adrenergic agonists.

scholarly journals Beta-adrenergic agonists increase maximal output of oxidative phosphorylation in bovine satellite cells1

2020 ◽  
Vol 4 (Supplement_1) ◽  
pp. S94-S97
Author(s):  
Renae L Sieck ◽  
Leah K Treffer ◽  
Martonio Ponte Viana ◽  
Oleh Khalimonchuk ◽  
Ty B Schmidt ◽  
...  
Keyword(s):  
Oxidative Phosphorylation ◽  
Adrenergic Agonists ◽  
Beta Adrenergic ◽  
Beta Adrenergic Agonists ◽  
Maximal Output

Interaction between the antidepressant-like behavioral effects of beta adrenergic agonists and the cyclic AMP PDE inhibitor rolipram in rats

2005 ◽  
Vol 182 (1) ◽  
pp. 104-115 ◽  
Author(s):  
Han-Ting Zhang ◽  
Ying Huang ◽  
Kathleen Mishler ◽  
Sandra C. Roerig ◽  
James M. O'Donnell
Keyword(s):  
Cyclic Amp ◽  
Behavioral Effects ◽  
Adrenergic Agonists ◽  
Beta Adrenergic ◽  
Beta Adrenergic Agonists
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