File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Pulmonary vasodilation to adrenomedullin: A novel peptide in humans

TitlePulmonary vasodilation to adrenomedullin: A novel peptide in humans
Authors
KeywordsChemicals And Cas Registry Numbers
Issue Date1995
PublisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpheart.physiology.org/
Citation
American Journal of Physiology - Heart and Circulatory Physiology, 1995, v. 268 n. 6 37-6, p. H2211-H2215 How to Cite?
AbstractThe present study investigates the effects of human adrenomedullin (ADM) on the pulmonary vascular bed of isolated, blood-perfused rat lung. Because pulmonary blood flow and left atrial pressure were constant, changes in pulmonary arterial pressure directly reflect changes in pulmonary vascular resistance. Under conditions of resting (low) pulmonary vasomotor tone, intra-arterial bolus injections of ADM-(1-52) and two truncated sequences of ADM-(1-52) [ADM-(1-12) and ADM-(13-52)] did not alter pulmonary arterial pressure. When pulmonary vasomotor tone was increased by U-46619, a thromboxane A2 mimic, intra-arterial bolus injections of ADM-(1-52) and ADM- (13-52) at similar doses produced similar, dose-dependent reductions in pulmonary arterial pressure. On a molar basis, ADM-(1-52) had greater pulmonary vasodilator activity than isoproterenol. In contrast, ADM-(1-12) had no activity. When pulmonary vasomotor tone was actively increased to the same level using KCl, the pulmonary vasodilator activity of ADM-(13-52) was decreased 10-fold. The present data demonstrate that ADM-(1-52) dilates the pulmonary vascular bed and suggest that the pulmonary vasodilator activity of ADM is greater on pulmonary blood vessels preconstricted through a receptor- dependent mechanism. Because meclofenamate, nitro-L-arginine methyl ester, methysergide, BW A-1433U83, U-37883A, and calcitonin gene-related peptide [CGRP-(8-37)], a CGRP-receptor antagonist, did not alter the pulmonary vasodilator response to ADM-(1-52), the present data suggest that ADM dilates the pulmonary vascular bed independently of cyclooxygenase products, endothelium-derived relaxation factor, serotoninergic receptors, adenosine1 purinoreceptors, ATP-dependent potassium channels, and CGRP receptors. Furthermore, only a fragment of the ADM molecule is necessary to dilate the pulmonary vascular bed. The present data suggest that ADM may represent a novel regulatory peptide in the lung.
Persistent Identifierhttp://hdl.handle.net/10722/91112
ISSN
2015 Impact Factor: 3.324
2015 SCImago Journal Rankings: 1.823

 

DC FieldValueLanguage
dc.contributor.authorHeaton, Jen_HK
dc.contributor.authorLin, Ben_HK
dc.contributor.authorChang, J-Ken_HK
dc.contributor.authorSteinberg, Sen_HK
dc.contributor.authorHyman, Aen_HK
dc.contributor.authorLippton, Hen_HK
dc.date.accessioned2010-09-17T10:13:13Z-
dc.date.available2010-09-17T10:13:13Z-
dc.date.issued1995en_HK
dc.identifier.citationAmerican Journal of Physiology - Heart and Circulatory Physiology, 1995, v. 268 n. 6 37-6, p. H2211-H2215en_HK
dc.identifier.issn0363-6135en_HK
dc.identifier.urihttp://hdl.handle.net/10722/91112-
dc.description.abstractThe present study investigates the effects of human adrenomedullin (ADM) on the pulmonary vascular bed of isolated, blood-perfused rat lung. Because pulmonary blood flow and left atrial pressure were constant, changes in pulmonary arterial pressure directly reflect changes in pulmonary vascular resistance. Under conditions of resting (low) pulmonary vasomotor tone, intra-arterial bolus injections of ADM-(1-52) and two truncated sequences of ADM-(1-52) [ADM-(1-12) and ADM-(13-52)] did not alter pulmonary arterial pressure. When pulmonary vasomotor tone was increased by U-46619, a thromboxane A2 mimic, intra-arterial bolus injections of ADM-(1-52) and ADM- (13-52) at similar doses produced similar, dose-dependent reductions in pulmonary arterial pressure. On a molar basis, ADM-(1-52) had greater pulmonary vasodilator activity than isoproterenol. In contrast, ADM-(1-12) had no activity. When pulmonary vasomotor tone was actively increased to the same level using KCl, the pulmonary vasodilator activity of ADM-(13-52) was decreased 10-fold. The present data demonstrate that ADM-(1-52) dilates the pulmonary vascular bed and suggest that the pulmonary vasodilator activity of ADM is greater on pulmonary blood vessels preconstricted through a receptor- dependent mechanism. Because meclofenamate, nitro-L-arginine methyl ester, methysergide, BW A-1433U83, U-37883A, and calcitonin gene-related peptide [CGRP-(8-37)], a CGRP-receptor antagonist, did not alter the pulmonary vasodilator response to ADM-(1-52), the present data suggest that ADM dilates the pulmonary vascular bed independently of cyclooxygenase products, endothelium-derived relaxation factor, serotoninergic receptors, adenosine1 purinoreceptors, ATP-dependent potassium channels, and CGRP receptors. Furthermore, only a fragment of the ADM molecule is necessary to dilate the pulmonary vascular bed. The present data suggest that ADM may represent a novel regulatory peptide in the lung.en_HK
dc.languageengen_HK
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpheart.physiology.org/en_HK
dc.relation.ispartofAmerican Journal of Physiology - Heart and Circulatory Physiologyen_HK
dc.subjectChemicals And Cas Registry Numbersen_HK
dc.titlePulmonary vasodilation to adrenomedullin: A novel peptide in humansen_HK
dc.typeArticleen_HK
dc.identifier.emailLin, B:blin@hku.hken_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.pmid7611471-
dc.identifier.scopuseid_2-s2.0-0028801711en_HK
dc.identifier.volume268en_HK
dc.identifier.issue6 37-6en_HK
dc.identifier.spageH2211en_HK
dc.identifier.epageH2215en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats