ENHANCEMENT OF PROSTAGLANDIN OUTPUT DURING ACTIVATION OF BETA-1 ADRENOCEPTORS IN THE ISOLATED RABBIT HEART

  • 1 January 1982
    • journal article
    • research article
    • Vol. 223  (3) , 729-735
Abstract
The type of adrenoceptor that mediates the effect of adrenergic stimuli on prostaglandin (PG) synthesis in the isolated rabbit heart was investigated and the relationship of the released PG to the mechanical changes elicited by catecholamines and stimulation of the cardiac sympathetic nerves was determined. 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 PG elicited by adrenergic stimuli. Indomethacin prevented the increase in PG formation caused by all stimuli. The adrenergically induced release of PG was not related to changes in heart rate, systolic tension or vascular tone elicited by the adrenergic stimuli. The adrenergically induced release of PG 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.

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