Document Detail

Effect of ghrelin on autonomic activity in healthy volunteers.
MedLine Citation:
PMID:  25265271     Owner:  NLM     Status:  Publisher    
Ghrelin is a novel growth hormone (GH)-releasing peptide originally isolated from the stomach. Recently, we have shown that ghrelin suppresses cardiac sympathetic activity and prevents early left ventricular remodeling in rats with myocardial infarction. In the present study, we evaluated the effect of ghrelin on autonomic nerve activity in healthy human subjects. An intravenous bolus of human synthetic ghrelin (10μg/kg) was administered to 10 healthy men (mean age, 33 years). Holter monitoring assessment was performed before and during 2hours after the ghrelin therapy. The standard deviation of normal RR intervals (SDNN), square root of the mean of the sum of the squares of differences between adjacent RR intervals (rMSSD), high-frequency power (HF), and low-frequency power (LF) were analyzed. Blood samples were also obtained before and after the therapy. A single administration of ghrelin decreased both heart rate and blood pressure. Interestingly, ghrelin significantly decreased the LF and LF/HF ratio of heart rate variability and increased the SDNN, rMSSD, and HF. Ghrelin also elicited a marked increase in circulating GH, but not insulin-like growth factor-1. These data suggest that ghrelin might suppress cardiac sympathetic nerve activity and stimulate cardiac parasympathetic nerve activity.
Takeshi Soeki; Kunihiko Koshiba; Toshiyuki Niki; Kenya Kusunose; Koji Yamaguchi; Hirotsugu Yamada; Tetsuzo Wakatsuki; Michio Shimabukuro; Kazuo Minakuchi; Ichiro Kishimoto; Kenji Kangawa; Masataka Sata
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2014-9-26
Journal Detail:
Title:  Peptides     Volume:  -     ISSN:  1873-5169     ISO Abbreviation:  Peptides     Publication Date:  2014 Sep 
Date Detail:
Created Date:  2014-9-29     Completed Date:  -     Revised Date:  2014-9-30    
Medline Journal Info:
Nlm Unique ID:  8008690     Medline TA:  Peptides     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2014. Published by Elsevier Inc.
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