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J Am Coll Cardiol, 2008; 52:908-913, doi:10.1016/j.jacc.2008.06.013
© 2008 by the American College of Cardiology Foundation
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CLINICAL RESEARCH: VASCULAR MEDICINE

Vascular Effects of Apelin In Vivo in Man

Alan G. Japp, MRCP*,*, Nicholas L. Cruden, PhD*, David A.B. Amer*, Vivienne K.Y. Li, BSc*, Ewan B. Goudie, BSc*, Neil R. Johnston, MSc*, Sushma Sharma, PhD{dagger}, Ilene Neilson, BSc{dagger}, David J. Webb, MD, FRCP*, Ian L. Megson, PhD{dagger}, Andrew D. Flapan, MD, MRCP{ddagger} and David E. Newby, PhD, FRCP*

* Centre for Cardiovascular Science, University of Edinburgh, Chancellor's Building, Edinburgh, United Kingdom
{dagger} Department of Diabetes, UHI Millennium Institute, Inverness, United Kingdom
{ddagger} Department of Cardiology, Royal Infirmary of Edinburgh, Edinburgh, United Kingdom

Manuscript received November 12, 2007; revised manuscript received March 26, 2008, accepted June 3, 2008.

* Reprint requests and correspondence: Dr. Alan G. Japp, Centre for Cardiovascular Science, The University of Edinburgh, Chancellor's Building, Edinburgh, EH16 4SB, United Kingdom (Email: alan.japp{at}ed.ac.uk).

Objectives: This study was designed to establish the direct vascular effects of apelin in vivo in man.

Background: Apelin is the endogenous ligand for the previously orphaned G-protein–coupled receptor, APJ. This novel pathway is widely expressed in the cardiovascular system and is emerging as an important mediator of cardiovascular homeostasis. In pre-clinical models, apelin causes venous and arterial vasodilation.

Methods: Vascular effects of apelin were assessed in 24 healthy volunteers. Dorsal hand vein diameter was measured by the Aellig technique during local intravenous infusions (0.1 to 3 nmol/min) of apelin-36, (Pyr1)apelin-13, and sodium nitroprusside (0.6 nmol/min). Forearm blood flow was measured by venous occlusion plethysmography during intrabrachial infusions of apelin-36 and (Pyr1)apelin-13 (0.1 to 30 nmol/min) and subsequently in the presence or absence of a "nitric oxide clamp" (nitric oxide synthase inhibitor, L-N G-monomethylarginine [8 µmol/min], coinfused with nitric oxide donor, sodium nitroprusside [90 to 900 ng/min]), or a single oral dose of aspirin (600 mg) or matched placebo.

Results: Although sodium nitroprusside caused venodilation (p < 0.0001), apelin-36 and (Pyr1)apelin-13 had no effect on dorsal hand vein diameter (p = 0.2). Both apelin isoforms caused reproducible vasodilation in forearm resistance vessels (p < 0.0001). (Pyr1)apelin-13–mediated vasodilation was attenuated by the nitric oxide clamp (p = 0.004) but unaffected by aspirin (p = 0.7).

Conclusions: Although having no apparent effect on venous tone, apelin causes nitric oxide–dependent arterial vasodilation in vivo in man. The apelin-APJ system merits further clinical investigation to determine its role in cardiovascular homeostasis.

Key Words: apelin • APJ receptor • endothelium • vasodilator

Abbreviations and Acronyms
  ANOVA = analysis of variance
  APJ = apelin receptor
  AUC = area under the curve
  DHV = dorsal hand vein
  FBF = forearm blood flow
  NO = nitric oxide
  SNP = sodium nitroprusside




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