Document Detail

Effects of beta adrenoceptor agonists and antagonists on adrenal catecholamine release in response to splanchnic nerve stimulation in anesthetized dogs: role of beta-1 and beta-2 adrenoceptors.
MedLine Citation:
PMID:  7791106     Owner:  NLM     Status:  MEDLINE    
The present study was performed to examine whether beta adrenoceptor agonists and antagonists modify the release of adrenal catecholamine (CA) in response to splanchnic nerve stimulation (SNS) in anesthetized dogs, in order to elucidate the beta adrenoceptor-mediated modulation of adrenal CA release. SNS at 3 Hz produced marked increases in both epinephrine and norepinephrine output determined from adrenal venous blood. Atenolol (10, 30 and 100 micrograms/kg, i.v.) and CGP20712A (10 and 30 micrograms/kg, i.v.), selective beta-1 adrenoceptor antagonists, significantly enhanced the SNS-induced increases in CA output. Neither ICI118551 (10, 30 and 100 micrograms/kg, i.v.), a selective beta-2 adrenoceptor antagonist, nor nadolol (10, 30 and 100 micrograms/kg, i.v.), a nonselective beta adrenoceptor antagonist, affected the SNS-induced increases in CA output. After the treatment with ICI118551 (100 micrograms/kg, i.v.), atenolol (10, 30 and 100 micrograms/kg, i.v.) failed to enhance the SNS-induced increases in CA output. On the other hand, neither isoproterenol (0.03 and 0.1 micrograms/kg/min, i.v.) nor the selective beta-2 adrenoceptor agonist procaterol (0.03 and 0.1 micrograms/kg/min, i.v.) affected the SNS-induced increases in CA output. After the treatment with atenolol (100 micrograms/kg, i.v.), both isoproterenol (0.03 micrograms/kg/min, i.v.) and procaterol (0.03 micrograms/kg/min, i.v.) enhanced the SNS-induced increases in CA output. The enhancing effects of isoproterenol and procaterol were abolished by ICI118551 (100 micrograms/kg, i.v.). These results indicate that activation of beta-2 adrenoceptors facilitates the SNS-evoked release of CA from the dog adrenal medulla under the condition in which beta-1 adrenoceptors are blocked, and they suggest that activation of beta-1 adrenoceptors inhibits the beta-2 adrenoceptor-mediated facilitation process of adrenal CA release.
H Koganei; T Kimura; S Satoh
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of pharmacology and experimental therapeutics     Volume:  273     ISSN:  0022-3565     ISO Abbreviation:  J. Pharmacol. Exp. Ther.     Publication Date:  1995 Jun 
Date Detail:
Created Date:  1995-07-21     Completed Date:  1995-07-21     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0376362     Medline TA:  J Pharmacol Exp Ther     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1337-44     Citation Subset:  IM    
Department of Pharmacology, Pharmaceutical Institute, Tohoku University, Sendai, Japan.
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MeSH Terms
Adrenal Glands / drug effects*,  metabolism
Adrenergic beta-Agonists / pharmacology*
Adrenergic beta-Antagonists / pharmacology*
Atenolol / pharmacology
Catecholamines / metabolism*
Imidazoles / pharmacology
Receptors, Adrenergic, beta-1 / metabolism
Receptors, Adrenergic, beta-2 / metabolism
Splanchnic Nerves / drug effects*,  metabolism
Reg. No./Substance:
0/Adrenergic beta-Agonists; 0/Adrenergic beta-Antagonists; 0/Catecholamines; 0/Imidazoles; 0/Receptors, Adrenergic, beta-1; 0/Receptors, Adrenergic, beta-2; 29122-68-7/Atenolol; 81015-67-0/CGP 20712A

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