Atrial Natriuretic Peptide Decreases Cardiac Output Independent of Coronary Vasoconstriction

John C. Burnett, Gabor M. Rubanyi, Brooks S. Edwards, Thomas R. Schwab, Robert S. Zimmerman, Paul M. Vanhoutte

Research output: Contribution to journalArticlepeer-review

18 Scopus citations


Studies were performed in isolated, Langendorff-perfused rat hearts and anesthetized dogs to determine the effects of synthetic atrial natriuretic peptide (ANP 8-33) on the coronary circulation. In vitro studies in the rat examined coronary flow dynamics to ANP 8-33 over a defined range from physiologic to pharmacologic concentrations. No changes in coronary flow or chronotropic and inotropic function of the isolated Langendorff-perfused heart were observed in response to increasing concentrations of ANP 8-33 (102 to 106 pg/ml). In the dog, a low, nonhypotensive dose of ANP 8-33 (0.05 μg/kg/min) decreased cardiac output with no change in coronary blood flow or coronary vascular resistance. At a high, hypotensive dose (0.3 μg/kg/min) ANP 8-33 decreased cardiac output in association with transient coronary vasodilation. Continued infusion resulted in a decrease in coronary blood flow and arterial pressure with no change in coronary vascular resistance. Thus, in vitro physiologic and pharmacologic concentrations of ANP, or in vivo low concentrations of ANP, do not result in an alteration in coronary flow. In vivo ANP 8-33, at both nonhypotensive and hypotensive concentrations, decreased cardiac output in the absence of coronary vasoconstriction.

Original languageEnglish (US)
Pages (from-to)313-318
Number of pages6
JournalProceedings of the Society for Experimental Biology and Medicine
Issue number3
StatePublished - Dec 1987

ASJC Scopus subject areas

  • General Biochemistry, Genetics and Molecular Biology


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