Facilitation of adrenergic transmission in the canine heart by intracoronary infusion of angiotensin II

Effect of prostaglandin synthesis inhibition

S. M. Lanier, Kafait Malik

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Abstract

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). AII 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 AII-induced increase in the coronary sinus output of NE and LVdP/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 AII 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. These data suggest that one or more products of arachidonic acid metabolism attenuate the facilitatory effect of AII on release of NE elicited by sympathetic nerve stimulation in the heart of anesthetized dogs.

Original languageEnglish (US)
Pages (from-to)676-682
Number of pages7
JournalJournal of Pharmacology and Experimental Therapeutics
Volume227
Issue number3
StatePublished - Dec 1 1983

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Angiotensin II
Adrenergic Agents
Prostaglandins
Canidae
Norepinephrine
Coronary Sinus
Indomethacin
Normetanephrine
Dogs
Prostaglandin Antagonists
Cyclooxygenase Inhibitors
Pentobarbital
Cocaine
Arachidonic Acid
Coronary Vessels

All Science Journal Classification (ASJC) codes

  • Molecular Medicine
  • Pharmacology

Cite this

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title = "Facilitation of adrenergic transmission in the canine heart by intracoronary infusion of angiotensin II: Effect of prostaglandin synthesis inhibition",
abstract = "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). AII 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 AII-induced increase in the coronary sinus output of NE and LVdP/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 AII 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. These data suggest that one or more products of arachidonic acid metabolism attenuate the facilitatory effect of AII on release of NE elicited by sympathetic nerve stimulation in the heart of anesthetized dogs.",
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T1 - Facilitation of adrenergic transmission in the canine heart by intracoronary infusion of angiotensin II

T2 - Effect of prostaglandin synthesis inhibition

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AU - Malik, Kafait

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N2 - 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). AII 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 AII-induced increase in the coronary sinus output of NE and LVdP/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 AII 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. These data suggest that one or more products of arachidonic acid metabolism attenuate the facilitatory effect of AII on release of NE elicited by sympathetic nerve stimulation in the heart of anesthetized dogs.

AB - 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). AII 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 AII-induced increase in the coronary sinus output of NE and LVdP/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 AII 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. These data suggest that one or more products of arachidonic acid metabolism attenuate the facilitatory effect of AII on release of NE elicited by sympathetic nerve stimulation in the heart of anesthetized dogs.

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