TY - JOUR
T1 - The Effects of Substance P on the Preconstricted Pulmonary Vasculature of the Anesthetized Dog
AU - Archer, S. L.
AU - Chesler, E.
AU - Weir, E. K.
AU - Kulik, T. J.
N1 - Copyright:
Copyright 2016 Elsevier B.V., All rights reserved.
PY - 1986/10
Y1 - 1986/10
N2 - Substance P is a vasoactive peptide. Nerve fibers containing substance P are present in the media of pulmonary arteries but the physiologic function of substance P in the pulmonary vasculature is unknown. Several doses of substance P were infused intravenously in the anesthetized dog to ascertain its effects on the pulmonary vasculature, both during normoxia and following preconstriction with hypoxia (F1O2 0.1) or prostaglandin F2α (PGF2α 5 μg/kg/min). Substance P resulted in systemic vasodilatation during normoxia but had minimal effect on the pulmonary vasculature. During hypoxia and PGF2α-induced pulmonary vasoconstriction, substance P significantly lowered pulmonary artery pressure, pulmonary vascular resistance, mean aortic pressure, and total systemic resistance. It had no effect on cardiac output, wedge pressure, and arterial blood gases. To investigate possible mechanisms for substance P-induced vasodilatation, substance P was studied following pretreatment with N-acetylcysteine (a radical scavenging agent), methylene blue (an inhibitor of guanylate cyclase), meclofenamate (a cyclooxygenase inhibitor), and atropine (a muscarinic receptor antagonist). None of these agents impaired substance P-induced vasodilatation. Substance P given intravenously is a nonselective vasodilator in the dog but the mechanism of its action remains uncertain.
AB - Substance P is a vasoactive peptide. Nerve fibers containing substance P are present in the media of pulmonary arteries but the physiologic function of substance P in the pulmonary vasculature is unknown. Several doses of substance P were infused intravenously in the anesthetized dog to ascertain its effects on the pulmonary vasculature, both during normoxia and following preconstriction with hypoxia (F1O2 0.1) or prostaglandin F2α (PGF2α 5 μg/kg/min). Substance P resulted in systemic vasodilatation during normoxia but had minimal effect on the pulmonary vasculature. During hypoxia and PGF2α-induced pulmonary vasoconstriction, substance P significantly lowered pulmonary artery pressure, pulmonary vascular resistance, mean aortic pressure, and total systemic resistance. It had no effect on cardiac output, wedge pressure, and arterial blood gases. To investigate possible mechanisms for substance P-induced vasodilatation, substance P was studied following pretreatment with N-acetylcysteine (a radical scavenging agent), methylene blue (an inhibitor of guanylate cyclase), meclofenamate (a cyclooxygenase inhibitor), and atropine (a muscarinic receptor antagonist). None of these agents impaired substance P-induced vasodilatation. Substance P given intravenously is a nonselective vasodilator in the dog but the mechanism of its action remains uncertain.
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U2 - 10.3181/00379727-183-42381
DO - 10.3181/00379727-183-42381
M3 - Article
C2 - 2428048
AN - SCOPUS:0022479065
SN - 0037-9727
VL - 183
SP - 19
EP - 27
JO - Proceedings of the Society for Experimental Biology and Medicine
JF - Proceedings of the Society for Experimental Biology and Medicine
IS - 1
ER -