PMID- 9384237
OWN - NLM
STAT- MEDLINE
DCOM- 19980122
LR  - 20190624
IS  - 0014-2999 (Print)
IS  - 0014-2999 (Linking)
VI  - 336
IP  - 2-3
DP  - 1997 Oct 8
TI  - Inhibitory mechanisms of beta-adrenoceptor agonists for immunoglobulin E-mediated 
      experimental allergic reactions in rats.
PG  - 225-31
AB  - Inhibitory mechanisms of isoproterenol and clenbuterol for immunoglobulin E 
      (IgE)-mediated experimental allergic reactions in rats were studied. IgE-mediated 
      passive cutaneous anaphylaxis, histamine-induced cutaneous reaction and 
      serotonin-induced cutaneous reaction were evoked at the same time in the same 
      rats. Isoproterenol administered intravenously immediately before challenge 
      inhibited all these reactions significantly. Clenbuterol administered 
      intravenously 0-3 h before challenge also significantly inhibited the three 
      cutaneous reactions. The inhibition was maximum when the drug was given 1 h 
      before challenge. Passive cutaneous anaphylaxis was always inhibited more 
      potently than histamine-induced cutaneous reaction and serotonin-induced 
      cutaneous reaction by these beta-adrenoceptor agonists. Passive peritoneal 
      anaphylaxis was caused by injecting an antigen intravenously. Isoproterenol 
      administered intravenously immediately before challenge inhibited the reaction 
      significantly. Clenbuterol administered intravenously 0-3 h before challenge also 
      significantly inhibited passive peritoneal anaphylaxis, maximally so when given 1 
      h before challenge. In vitro IgE-dependent histamine release from sensitized 
      peritoneal mast cells or mesenteric mast cells was not affected by isoproterenol 
      and clenbuterol. Mouse monoclonal IgE, a foreign protein, administered 
      intravenously decreased rapidly in the circulation. About 50% of the mouse IgE 
      given disappeared in 20 min. The decrease of mouse IgE was partly but 
      significantly inhibited by the beta-adrenoceptor agonists, and the inhibition was 
      abolished by simultaneous treatment with propranolol. These results indicate that 
      direct inhibition of mast cell activation does not contribute to the potent 
      inhibition of in vivo allergic reactions in rats by beta-adrenoceptor agonists, 
      and that inhibition of the allergic cutaneous reaction is partially explained by 
      the inhibition of vascular permeability increases caused by mast cell mediators. 
      Penetration of intravenously administered antigen from blood vessels to 
      peripheral tissues to cause mast cell activation might be inhibited by 
      beta-adrenoceptor agonists, and this could play some role in inhibiting 
      intravenous antigen-induced allergic reactions in rats. Clenbuterol exhibited its 
      maximum action with some latency in vivo, suggesting that some time-requiring 
      process may be involved in the manifestation of its action.
FAU - Inagaki, N
AU  - Inagaki N
AD  - Department of Pharmacology, Gifu Pharmaceutical University, Japan.
FAU - Kawasaki, H
AU  - Kawasaki H
FAU - Hiyama, H
AU  - Hiyama H
FAU - Goto, M
AU  - Goto M
FAU - Matsuo, A
AU  - Matsuo A
FAU - Nagai, H
AU  - Nagai H
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PL  - Netherlands
TA  - Eur J Pharmacol
JT  - European journal of pharmacology
JID - 1254354
RN  - 0 (Adrenergic beta-Agonists)
RN  - 37341-29-0 (Immunoglobulin E)
RN  - L628TT009W (Isoproterenol)
RN  - XTZ6AXU7KN (Clenbuterol)
SB  - IM
MH  - Adrenergic beta-Agonists/*therapeutic use
MH  - Animals
MH  - Clenbuterol/*therapeutic use
MH  - Histamine Release/drug effects
MH  - Hypersensitivity, Immediate/*prevention & control
MH  - Immunoglobulin E/metabolism
MH  - Isoproterenol/*therapeutic use
MH  - Male
MH  - Mast Cells/*drug effects/metabolism
MH  - Mice
MH  - Rats
MH  - Rats, Wistar
EDAT- 1998/01/24 00:00
MHDA- 1998/01/24 00:01
CRDT- 1998/01/24 00:00
PHST- 1998/01/24 00:00 [pubmed]
PHST- 1998/01/24 00:01 [medline]
PHST- 1998/01/24 00:00 [entrez]
AID - S0014-2999(97)01247-8 [pii]
AID - 10.1016/s0014-2999(97)01247-8 [doi]
PST - ppublish
SO  - Eur J Pharmacol. 1997 Oct 8;336(2-3):225-31. doi: 10.1016/s0014-2999(97)01247-8.