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.
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.
Koganei
H
H
Department of Pharmacology, Pharmaceutical Institute, Tohoku University, Sendai, Japan.
Kimura
T
T
Satoh
S
S
D000311:Adrenal Glands / Q000187:drug effects* / Q000378:metabolism; D000318:Adrenergic beta-Agonists / Q000494:pharmacology*; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology*; D000818:Animals; D001262:Atenolol / Q000494:pharmacology; D002395:Catecholamines / Q000378:metabolism*; D004285:Dogs; D005260:Female; D007093:Imidazoles / Q000494:pharmacology; D008297:Male; D018342:Receptors, Adrenergic, beta-1 / Q000378:metabolism; D018343:Receptors, Adrenergic, beta-2 / Q000378:metabolism; D013153:Splanchnic Nerves / Q000187:drug effects* / Q000378:metabolism
D000318:Adrenergic beta-Agonists; D000319:Adrenergic beta-Antagonists; D002395:Catecholamines; D007093:Imidazoles; D018342:Receptors, Adrenergic, beta-1; D018343:Receptors, Adrenergic, beta-2; D001262:Atenolol; C049763:CGP 20712A