| Myocardial contractile effects of L-arginine in the human allograft. | |
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MedLine Citation:
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PMID: 9137232 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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OBJECTIVES: In the present study, we investigated, in transplant recipients, whether L-arginine (L-arg) potentiates the myocardial contractile effects of receptor-mediated coronary endothelial stimulation. Moreover, because inducible nitric oxide synthase (iNOS) is frequently expressed in transplanted myocardium, we also performed intracoronary infusion of L-arg in the absence of receptor-mediated coronary endothelial stimulation to investigate whether similar left ventricular (LV) contractile effects could be induced by providing more substrate for iNOS. BACKGROUND: Nitric oxide (NO), released from coronary endothelium after receptor-mediated stimulation by substance P (SP), affects vascular smooth muscle tone and modulates LV contractile performance. L-arg augments receptor-mediated endothelium-dependent coronary vasodilation in transplant recipients by increasing substrate availability for endothelial NO production. METHODS: Sixteen transplant recipients were studied at the time of annual coronary angiography. In eight transplant recipients, microtip LV pressures were recorded before and during intracoronary (IC) SP (20 pmol/min) and after the addition of IC L-arg (160 mumol/min) to IC SP. In eight transplant recipients, microtip LV pressures were recorded before and during IC L-arg (160 mumol/min) alone, and in six of these patients, endomyocardial biopsy samples were obtained to detect the expression of iNOS gene by reverse transcription-polymerase chain reaction. RESULTS: Addition of IC L-arg to IC SP induced a fall (mean +/- SEM) in LV peak systolic pressure (-16 +/- 4 mm Hg), which was larger (p < 0.01) than that observed during IC SP (-7 +/- 2 mm Hg). During IC L-arg alone, there was no change in LV peak systolic pressure despite the presence of iNOS mRNA in five of the six biopsy samples. CONCLUSIONS: In transplant recipients, L-arg potentiates the paracrine myocardial contractile effects of receptor-mediated coronary endothelial stimulation, probably by providing more substrate for endothelial NO production. Despite the myocardial expression of iNOS gene, L-arg alone fails to elicit similar contractile effects. |
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Authors:
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W J Paulus; S Kästner; M Vanderheyden; A M Shah; H Drexler |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Journal of the American College of Cardiology Volume: 29 ISSN: 0735-1097 ISO Abbreviation: J. Am. Coll. Cardiol. Publication Date: 1997 May |
Date Detail:
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Created Date: 1997-06-03 Completed Date: 1997-06-03 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 8301365 Medline TA: J Am Coll Cardiol Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 1332-8 Citation Subset: AIM; IM |
Affiliation:
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Cardiovascular Center, O.L.V. Ziekenhuis, Aalst, Belgium. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Arginine
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pharmacology* Coronary Angiography Endothelium, Vascular / metabolism*, physiology Female Heart Catheterization Heart Transplantation / physiology* Humans Infusions, Intra-Arterial Male Middle Aged Myocardial Contraction / drug effects* Nitric Oxide / biosynthesis, physiology* Nitric Oxide Synthase / biosynthesis, physiology* Polymerase Chain Reaction RNA, Messenger / genetics Substance P / pharmacology Ventricular Function, Left / drug effects Ventricular Pressure / drug effects |
| Chemical | |
Reg. No./Substance:
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0/RNA, Messenger; 10102-43-9/Nitric Oxide; 33507-63-0/Substance P; 74-79-3/Arginine; EC 1.14.13.39/Nitric Oxide Synthase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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