Inhibitory Effects of β-Adrenergic Stimulants on Increased Vascular Permeability Caused by Passive Cutaneous Anaphylaxis, Allergic Mediators, and Mediator Releasers in Rats

Pharmacology ◽  
1989 ◽  
Vol 39 (1) ◽  
pp. 19-27 ◽  
Author(s):  
Naoki Inagaki ◽  
Toru Miura ◽  
Michio Daikoku ◽  
Hiroichi Nagai ◽  
Akihide Koda
Keyword(s):  
Vascular Permeability ◽  
Passive Cutaneous Anaphylaxis ◽  
Inhibitory Effects ◽  
Beta Adrenergic

Compounds that increase cAMP prevent ischemia-reperfusion pulmonary capillary injury

1992 ◽  
Vol 72 (2) ◽  
pp. 492-497 ◽  
Author(s):  
W. K. Adkins ◽  
J. W. Barnard ◽  
S. May ◽  
A. F. Seibert ◽  
J. Haynes ◽  
...  
Keyword(s):  
Adenylate Cyclase ◽  
Vascular Permeability ◽  
Vascular Resistance ◽  
Capillary Permeability ◽  
Ischemia Reperfusion ◽  
Receptor Activation ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Beta Receptor ◽  
Pulmonary Capillary

This study evaluated the physiological effects of compounds that increase adenosine 3′,5′-cyclic monophosphate (cAMP) on changes in pulmonary capillary permeability and vascular resistance induced by ischemia-reperfusion (I-R) in isolated blood-perfused rabbit lungs. cAMP was elevated by 1) beta-adrenergic stimulation with isoproterenol (ISO, 10(-5) M), 2) post-beta-receptor stimulation of adenylate cyclase with forskolin (FSK, 10(-5) M), 3) and dibutyryl cAMP (DBcAMP, 1 mM), a cAMP analogue. Vascular permeability was assessed by determining the capillary filtration coefficient (Kf,c), and capillary pressure was measured using the double occlusion technique. The total, arterial, and venous vascular resistances were calculated from measured pulmonary arterial, venous, and capillary pressures and blood flow. Reperfusion after 2 h of ischemia significantly (P less than 0.05) increased Kf,c (from 0.115 +/- 0.028 to 0.224 +/- 0.040 ml.min-1.cmH2O-1.100 g-1). These I-R-induced changes in capillary permeability were prevented when ISO, FSK, or DBcAMP was added to the perfusate at reperfusion (0.110 +/- 0.022 and 0.103 +/- 0.021, 0.123 +/- 0.029 and 0.164 +/- 0.024, and 0.153 +/- 0.030 and 0.170 +/- 0.027 ml.min-1.cmH2O-1.100 g-1, respectively). I-R significantly increased total, arterial, and venous vascular resistances. These increases in vascular resistance were also blocked by ISO, FSK, and DBcAMP. These data suggest that beta-adrenergic stimulation, post-beta-receptor activation of adenylate cyclase, and DBcAMP prevent the changes in pulmonary vascular permeability and vascular resistances caused by I-R in isolated rabbit lungs through a mechanism involving an increase in intracellular levels of cAMP.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of beta-adrenergic receptor activation on alveolar macrophage cytoplasmic motility

1993 ◽  
Vol 265 (1) ◽  
pp. L67-L72 ◽  
Author(s):  
T. Fukushima ◽  
K. Sekizawa ◽  
Y. Jin ◽  
M. Yamaya ◽  
H. Sasaki ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Adrenergic Receptor ◽  
Specific Inhibitor ◽  
Lower Lobe ◽  
Receptor Activation ◽  
Maximum Effect ◽  
Inhibitory Effects ◽  
Particle Rotation ◽  
Beta Adrenergic Receptor ◽  
Beta Adrenergic

We studied the effects of fenoterol, a beta-adrenoceptor agonist, on the cytoplasmic motility of alveolar macrophages (AM) from dog lungs in vitro. Four days after the instillation of Fe3O4 particles (3 mg/kg) into the lower lobe bronchus, AM were harvested by bronchoalveolar lavage. Remanent field strength (RFS) from the AM containing Fe3O4 particles (5 x 10(6) cells) was measured immediately after magnetization. RFS decreased with time due to particle rotation (relaxation), which is related to cytoplasmic motility of AM. Fenoterol (10(-9) M to 10(-5) M) decreased the relaxation rate (lambda 0; min-1) in a concentration-dependent fashion with the maximum effect at 10(-6) M. Both forskolin (10(-6) M to 10(-4) M) and dibutyryl adenosine 3',5'-cyclic monophosphate (cAMP) (10(-3) M) mimicked fenoterol-induced inhibitory effects on lambda 0. Fenoterol and forskolin concentration-dependently increased intracellular levels of cAMP, which were parallel to decreases in lambda 0 induced by these drugs. KT 5720 (10(-5) M), a specific inhibitor of protein kinase A, significantly inhibited fenoterol (10(-6) M)-induced inhibitory effects on lambda 0 (P < 0.01). These results imply that beta-adrenergic receptor activation inhibits cytoplasmic motility of AM via increases in intracellular levels of cAMP, which may be coupled with activation of a cAMP-dependent protein kinase.

Inhibitory effects of beta-adrenergic agonists on gastric acid secretion in dogs

1986 ◽  
Vol 251 (4) ◽  
pp. G453-G459
Author(s):  
M. H. Stevens ◽  
R. C. Thirlby ◽  
C. T. Richardson ◽  
M. A. Fredrickson ◽  
R. H. Unger ◽  
...  
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Intravenous Infusion ◽  
Acid Output ◽  
Gastric Fistula ◽  
Adrenergic Agonists ◽  
Inhibitory Effects ◽  
Beta Adrenergic ◽  
Beta Adrenergic Agonists

We evaluated the effect of two beta-adrenergic agonists, isoproterenol (nonselective agonist) and terbutaline (selective beta 2-agonist), on gastric acid secretion stimulated by intravenous pentagastrin, bethanechol, or histamine in dogs with gastric fistulas. Intravenous infusion of isoproterenol or terbutaline inhibited pentagastrin-stimulated acid secretion to a significantly greater extent than they inhibited bethanechol- or histamine-stimulated acid secretion. For example, isoproterenol (12 micrograms X kg-1 X h-1) reduced mean pentagastrin-, bethanechol-, and histamine-stimulated acid output by 86, 63, and 14%, respectively. Percent inhibition of acid secretion with terbutaline (30 micrograms X kg-1 X h-1) averaged 60, 17, and 24% for pentagastrin, bethanechol, and histamine, respectively. Terbutaline also inhibited pentagastrin-stimulated acid secretion from vagally denervated fundic pouches in a dose-related manner. Plasma somatostatin-like immunoreactivity was significantly higher during infusion of terbutaline plus pentagastrin than during infusion of pentagastrin alone. However, an intravenous infusion of 0.3 microgram X kg-1 X h-1 somatostatin-14 had no effect on pentagastrin-stimulated acid secretion from the gastric fistula, even though this infusion increased plasma somatostatin-like immunoreactivity to the same extent as terbutaline plus pentagastrin infusion. Thus the amount of somatostatin released during terbutaline infusion was not sufficient to explain the inhibition of pentagastrin-stimulated acid secretion observed.

scholarly journals Attenuated Zymosan-induced Peritoneal Vascular Permeability and IgE-dependent Passive Cutaneous Anaphylaxis in Mice Lacking Leukotriene C4Synthase

2001 ◽  
Vol 276 (25) ◽  
pp. 22608-22613 ◽  
Author(s):  
Yoshihide Kanaoka ◽  
Akiko Maekawa ◽  
John F. Penrose ◽  
K. Frank Austen ◽  
Bing K. Lam
Keyword(s):  
Vascular Permeability ◽  
Passive Cutaneous Anaphylaxis
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