Hydrocortisone and isoproterenol effects on trachealis cAMP and relaxation

1983 ◽  
Vol 55 (5) ◽  
pp. 1609-1613 ◽  
Author(s):  
G. A. Rinard ◽  
A. Jensen ◽  
A. M. Puckett
Keyword(s):  
Smooth Muscle ◽  
Muscle Relaxation ◽  
Adrenergic Agonist ◽  
Response Curves ◽  
Beta Adrenergic ◽  
Cyclic Monophosphate ◽  
Beta Adrenergic Agonists ◽  
Beta Adrenergic Agonist ◽  
Camp Formation ◽  
Hydrocortisone Treatment

Isoproterenol concentration-response curves for cAMP formation and relaxation were determined in control and hydrocortisone-treated strips of canine tracheal smooth muscle. Adenosine 3′5′-cyclic monophosphate(cAMP) formation and muscle relaxation were well correlated, and both responses were enhanced proportionally by hydrocortisone treatment. Guanosine 3′5′-cyclic monophosphate was unchanged by isoproterenol but was increased to a small but significant extent by hydrocortisone. Prostaglandin E2 (not a beta-adrenergic agonist) relaxed the muscle strips, but this effect was not enhanced by hydrocortisone pretreatment. Our data are compatible with the concept that cAMP is an obligatory intermediate in the chain of events by which beta-adrenergic agonists relax airway smooth muscle. The action of hydrocortisone on this process is localized at or before cAMP formation, since it enhanced both cAMP formation and relaxation to the same extent.

Effect of adrenergic agonists on big and small renin

1980 ◽  
Vol 238 (5) ◽  
pp. E416-E420
Author(s):  
H. Iwao ◽  
C. S. Lin ◽  
A. M. Michelakis
Keyword(s):  
Submaxillary Gland ◽  
Plasma Renin ◽  
Adrenergic Agonists ◽  
Adrenergic Agonist ◽  
Beta Adrenergic ◽  
Molecular Weights ◽  
Submaxillary Glands ◽  
Beta Adrenergic Agonists ◽  
Beta Adrenergic Agonist ◽  
Alpha Adrenergic Agonist

The effect of alpha- and beta-adrenergic agonists on renal and submaxillary renin of different molecular weights was studied using male albino mice as experimental animals. Phenylephrine or isoproterenol was administered intravenously after removal of the submaxillary glands and/or kidneys. Renin was isolated from plasma by column chromatography and then measured by a direct radioimmunoassay. Phenylephrine increased both 68,500-dalton renin (big renin) and 38,000-dalton renin (small renin) in the plasma of nephrectomized mice. Isoproterenol increased big and small renin in the plasma of mice whose submaxillary glands were removed. In both cases, the increase of small renin was significantly greater than that of big renin. The results suggest that the alpha-adrenergic agonist phenylephrine affects the submaxillary gland, leading to the increase of both big and small plasma renin. In contrast, the beta-adrenergic agonist isoproterenol affects the kidney, leading to the increase of both big and small plasma renin.

The effect of feeding the beta-adrenergic agonist ractopamine on the behaviour of market-weight pigs

1992 ◽  
Vol 72 (1) ◽  
pp. 15-21 ◽  
Author(s):  
A. L. Schaefer ◽  
S. D. M. Jones ◽  
A. K. W. Tong ◽  
A. M. B. dePassille ◽  
J. Rushen ◽  
...  
Keyword(s):  
Aggressive Behaviour ◽  
Adrenergic Agonists ◽  
Adrenergic Agonist ◽  
Beta Adrenergic ◽  
Treatment Groups ◽  
Beta Adrenergic Agonists ◽  
Key Words Pig ◽  
Ad Libitum ◽  
Beta Adrenergic Agonist ◽  
Effect Of Feeding

A total of 86 ad libitum fed Lacombe bred barrows and gilts weighing on average 90 kg were used to determine the effect of feeding ractopamine on animal behaviour. Four treatment groups consisted of a control (N = 22) and three levels of ractopamine (10 ppm (N = 15), 15 ppm (N = 24) and 20 ppm (N = 25) in the diet). The pigs received the ractopamine treatments for 5–6 wk prior to behavioural observations. There was little effect of ractopamine on behaviour. The ractopamine-fed pigs were observed to lie down in a group more frequently (P = 0.06) and to walk around their pen less frequently (P = 0.01). No abnormal, stereotyped, agonistic or aggressive behaviour was induced by the ractopamine. The data from the present study suggest that ractopamine, added to the diet of market-weight pigs at levels reported, does not cause marked changes in behaviour. Key words: Pig behaviour, beta-adrenergic agonists, ractopamine

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

Changes in vascular responsiveness following chronic exposure to cold in the rat

1983 ◽  
Vol 55 (3) ◽  
pp. 823-829 ◽  
Author(s):  
B. A. Bryar ◽  
M. J. Fregly ◽  
F. P. Field
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscles ◽  
Aortic Tissue ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Aortic Smooth Muscle ◽  
Beta Adrenergic Agonists ◽  
Adrenergic Antagonist ◽  
Vascular Responsiveness ◽  
High Concentrations

The responsiveness of smooth muscle from rings of aortic tissue of cold-acclimated (CA, 6 degrees C, 5-15 wk) rats to both alpha- and beta-adrenergic agonists and KCl was tested and compared with that of warm-adapted (25 degrees C) controls. alpha-Adrenergic stimulation, induced by low doses (10(-8)-10(-7) M) of phenylephrine and norepinephrine in the presence and absence of the beta-adrenergic antagonist, propranolol, resulted in the development of less active tension by aortic smooth muscle from CA rats than from controls. Similar results were observed with the weakly alpha 1-adrenergic agonistic activities of tyramine, clonidine, and high concentrations of isoproterenol (10(-6)-10(-4) M). There was also a significant reduction in the tension developed by smooth muscles of the aortas from CA rats when depolarized with KCl in concentrations ranging from 8 to 20 mM. In contrast, aortic smooth muscle, contracted to 75% of maximum with KCl, showed an enhanced relaxation to the beta-adrenergic agonist, isoproterenol, in CA rats. These studies suggest that acclimation of rats to cold results in both a decrease in alpha-adrenergic responsiveness and an increase in beta-adrenergic responsiveness in vascular smooth muscle as well as a change in the biochemical events that couple activation of adrenergic receptors to changes in vasomotor tone.

Transforming growth factor-alpha increases alveolar liquid clearance in anesthetized ventilated rats

1996 ◽  
Vol 271 (2) ◽  
pp. L236-L244 ◽  
Author(s):  
H. G. Folkesson ◽  
J. F. Pittet ◽  
G. Nitenberg ◽  
M. A. Matthay
Keyword(s):  
Transforming Growth Factor ◽  
Adrenergic Agonist ◽  
Beta Adrenergic ◽  
Alveolar Epithelial ◽  
Factor Alpha ◽  
Beta Adrenergic Agonist ◽  
Camp Levels ◽  
Na Uptake ◽  
Alveolar Liquid Clearance ◽  
Alveolar Liquid

The effect of transforming growth factor-alpha (TGF-alpha) on alveolar liquid clearance was examined in ventilated, anesthetized rats. An isosmolar Ringer lactate solution with 10, 50, or 200 ng/ml TGF-alpha and 125I-labeled albumin as the alveolar protein tracer was instilled into the right lower lung lobe; the rats were studied for 1 and 4 h. Compared with control rats, addition of 50 ng/ml TGF-alpha to the instilled fluid increased alveolar liquid clearance by 47% over 1 h and by 66% over 4 h (P < 0.05). This increase was similar to the 50% increase in alveolar liquid clearance over 1 h in rats instilled with a beta-adrenergic agonist, salmeterol (28). There was a dose-dependent effect of TGF-alpha (10, 50, 200 ng/ml) on alveolar liquid clearance. The combination of both TGF-alpha and salmeterol did not have an additive effect on alveolar liquid clearance. The TGF-alpha-stimulated increase in alveolar liquid clearance was inhibited by amiloride (10(-4) M), indicating that the increase in clearance depended on increased Na+ uptake across the alveolar epithelium. There was only a twofold increase in intracellular cAMP levels in isolated rat alveolar epithelial type II cells after stimulation with TGF-alpha. In contrast, beta-adrenergic agonist treatment increased intracellular adenosine 3',5'-cyclic monophosphate (cAMP) levels more than tenfold. Genistein (10(-6) M), a tyrosine protein kinase inhibitor, inhibited the TGF-alpha-stimulated increase in alveolar liquid clearance. In summary, TGF-alpha can stimulate in vivo alveolar liquid clearance at a rate similar to beta-adrenergic stimulation by increasing Na+ uptake by alveolar epithelial type II cells. However, the effect may be mediated by a non-cAMP dependent mechanism. Because genistein blocked the increase in alveolar fluid clearance, the signal transduction may involve genistein-dependent phosphorylation.

Sign in / Sign up

Export Citation Format

Share Document