Uptake and Effects of the Beta‐Adrenergic Agonist Salbutamol in Fish: Supporting Evidence for the Fish Plasma Model

2019 ◽  
Vol 38 (11) ◽  
pp. 2509-2519
Author(s):  
Mirco Weil ◽  
Anna‐Maria Falkenhain ◽  
Marco Scheurer ◽  
Jim J. Ryan ◽  
Anja Coors
Keyword(s):  
Supporting Evidence ◽  
Plasma Model ◽  
Adrenergic Agonist ◽  
Beta Adrenergic ◽  
Beta Adrenergic Agonist

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.

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.

Activity fronts in fed dogs: effect of a beta-adrenergic agonist

1983 ◽  
Vol 245 (5) ◽  
pp. G647-G650
Author(s):  
R. Yanda ◽  
R. W. Summers
Keyword(s):  
Motor Activity ◽  
Terminal Ileum ◽  
Phase Iii ◽  
Myoelectric Activity ◽  
Adrenergic Agonist ◽  
Beta Adrenergic ◽  
Induced Hypotension ◽  
Fasted State ◽  
Beta Adrenergic Agonist ◽  
Isoproterenol Infusion

The effect of the beta-adrenergic agonist isoproterenol on intestinal myoelectric activities was studied in fed dogs. A 15-min isoproterenol infusion (0.5 micrograms X kg-1 X min-1) initiated activity fronts after a meal in 14 of 16 experiments. The phase III motor activity was of similar duration and migrated aborally at the same rate as spontaneous fronts occurring in the interdigestive period; however, the activity fronts usually originated in the midjejunum and seldom migrated to the terminal ileum. The isoproterenol-induced fronts were blocked by pretreatment with propranolol (1 mg/kg). Activity fronts were not induced by sodium nitroprusside (10 micrograms X kg-1 X min-1), even though it inhibited myoelectric activity and induced hypotension and tachycardia to a degree similar to that caused by isoproterenol. The effects of isoproterenol were not blocked by vagotomy. Longer isoproterenol infusions of 2 h produced one but not more activity fronts and infusions in the fasted state did not induce premature fronts. These results do not support the hypothesis that the effect of isoproterenol is due to a neural reflex, and further studies are necessary to determine which of several potential mechanisms is responsible for this effect.

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