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SM Lanier and KU Malik
We studied the effect of intracoronary angiotensin II (AII) infusion on the coronary sinus output of norepinephrine (NE) elicited by left cardiac sympathetic nerve stimulation in pentobarbital-anesthetized dogs pretreated with a prostaglandin synthesis inhibitor (indomethacin) or its vehicle. The NE output from the heart was determined from the NE levels in coronary sinus blood before and during cardiac sympathetic nerve stimulation. In both indomethacin- and vehicle-pretreated animals, infusion of AII (30 ng kg-1 min-1) into the left coronary artery augmented the coronary sinus output of NE elicited by sympathetic nerve stimulation, but had no effect on the basal output of NE from the heart. In both groups of animals, the AII-induced increase in NE output was associated with an increase in the effect of cardiac sympathetic nerve stimulation on left ventricular contractility (LVdP/dt max). All did not alter the removal of exogenous NE by the heart and moreover the AII-induced increase in the output of NE elicited by cardiac sympathetic nerve stimulation was also observed during blockade of neuronal and extraneuronal uptake with cocaine and normetanephrine, respectively. Therefore, the All-induced increase in the coronary sinus output of NE and LVdPl dt max elicited by cardiac sympathetic nerve stimulation is most likely due to enhanced NE release from adrenergic nerve terminals in the heart. The ability of All to increase the coronary sinus output of NE and the positive inotropic response elicited by cardiac sympathetic nerve stimulation was enhanced in animals pretreated with the cyclooxygenase inhibitor, indomethacin.(ABSTRACT TRUNCATED AT 250 WORDS)
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