Hypoxia enhances isoproterenol-induced increase in heart interstitial adenosine, depressing beta-adrenergic contractile responses.

摘要: Endogenous interstitial adenosine may protect the hypoxic heart by attenuating beta-adrenergic-induced contractile and metabolic responses, thereby reducing energy utilization. Constant-flow perfused rat hearts were used to study: 1) effect of hypoxia on isoproterenol (ISO)-induced increase in adenosine, as estimated with epicardial surface transudates, 2) role endogenous depression ISO-induced responses. ISO (1 nM for 10 minutes) normoxic increased transudate 114% from a pre-ISO value 343 pmol/ml. administered 357% 797 The absolute magnitude was 625% greater during than normoxia. This associated reduction response hypoxia. In other experiments, normoxia (10 seconds) developed left ventricular pressure 140 mm Hg, maximum rates development relaxation 5,860 2,771 Hg/sec, respectively, above control values 90 2,250 1,875 Hg/sec. Hypoxia reduced three responses 50%, 56%, 36%. However, 1,3-dipropyl-8-cyclopentylxanthine (5 x 10(-7) M), an A1-receptor antagonist, added resulted only 31%, 39%, 9% relaxation, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)