PT  - JOURNAL ARTICLE
AU  - J E Shaffer
AU  - K U Malik
TI  - Enhancement of prostaglandin output during activation of beta-1 adrenoceptors in the isolated rabbit heart.
DP  - 1982 Dec 01
TA  - Journal of Pharmacology and Experimental Therapeutics
PG  - 729--735
VI  - 223
IP  - 3
4099  - http://jpet.aspetjournals.org/content/223/3/729.short
4100  - http://jpet.aspetjournals.org/content/223/3/729.full
SO  - J Pharmacol Exp Ther1982 Dec 01; 223
AB  - The purpose of this study was to elucidate the type of adrenoceptor that mediates the effect of adrenergic stimuli on prostaglandin (PG) synthesis in the isolated rabbit heart and to determine the relationship of the released PGs to the mechanical changes elicited by catecholamines and stimulation of the cardiac sympathetic nerves. The output of 6-keto PGF1 alpha, PGE2 and PGF2 alpha was increased by electrical stimulation of the sympathetic nerves, norepinephrine, isoproterenol, dobutamine and angiotensin II, but not by phenylephrine or isoetharine. Propranolol or atenolol, but not phentolamine or butoxamine, blocked the output of PGs elicited by adrenergic stimuli. Indomethacin prevented the increase in PG formation caused by all stimuli. Moreover, the adrenergically induced release of PGs was not related to changes in heart rate, systolic tension or vascular tone elicited by the adrenergic stimuli. These data indicate that the adrenergically induced release of PGs in the isolated rabbit heart is due to the activation of beta-1 adrenoceptors and is independent of the mechanical effects produced by the adrenergic stimuli.