The effects of a growth hormone-releasing hormone antagonist and a gastrin-releasing peptide antagonist on intimal hyperplasia of the carotid artery after balloon injury in a diabetic rat model☆

Bibliographic Details
Title: The effects of a growth hormone-releasing hormone antagonist and a gastrin-releasing peptide antagonist on intimal hyperplasia of the carotid artery after balloon injury in a diabetic rat model☆
Authors: John C. Moscona, Matthew N. Peters, Andrew V. Schally, Sudesh Srivastav, Patrice Delafontaine, Anand Irimpen
Source: Artery Research, Vol 19 (2017)
Publisher Information: BMC, 2017.
Publication Year: 2017
Collection: LCC:Specialties of internal medicine
LCC:Diseases of the circulatory (Cardiovascular) system
Subject Terms: Neointimal hyperplasia, Growth hormone-releasing hormone antagonist, Gastrin-releasing peptide antagonist, Arterial restenosis, Diabetes mellitus, Specialties of internal medicine, RC581-951, Diseases of the circulatory (Cardiovascular) system, RC666-701
More Details: Introduction: Arterial restenosis after angioplasty/stenting has hindered coronary artery disease treatment, especially in diabetics. We theorized that gastrin-releasing peptide (GRP) antagonists and growth hormone-releasing hormone (GHRH) antagonists might decrease neointimal hyperplasia and restenosis in diabetic rats after common carotid arterial balloon injury. Methods: Two separate experiments were conducted to test the effects of a GRP antagonist (RC-3095) and a GHRH antagonist (MZ-4-71) on vascular smooth muscle (VSM) growth. In a preliminary in vitro experiment non-injured human aortic vascular smooth muscle (VSM) proliferation was compared between growth media and control. In a second in vivo experiment, intimal and medial area, intima/media ratio (IM) and percent stenosis were compared between injured carotid arteries in twelve Zucker type II obese rats treated with subcutaneously injected RC-3095, MZ-4-71, or control media. Results: In the in vitro experiment, decreased VSM cell growth was observed in GRP antagonist (p < 0.05) and GHRH antagonist groups (p < 0.05) compared to the control group. In the in vivo experiment, the GRP antagonist group had a decreased IM ratio (1.63 ± 0.41, p < 0.05) and an increased area of stenosis (98.78% ± 1.48 p = NS) compared to control (2.38 ± 1.09) while the GHRH antagonist group had decreased IM ratio (1.33 ± 0.58 SD, p < 0.05) and percent area of stenosis (78.84% ± 24.97, p < 0.05) compared to control (2.38 ± 1.09). Conclusions: The significant decrease in both IM ratio and percent area of stenosis in the GHRH antagonist group supports the hypothesis that this peptide may reduce neointimal hyperplasia and restenosis.
Document Type: article
File Description: electronic resource
Language: English
ISSN: 12592498
1876-4401
Relation: https://www.atlantis-press.com/article/125924982/view; https://doaj.org/toc/1876-4401
DOI: 10.1016/j.artres.2017.06.006
Access URL: https://doaj.org/article/f1db94ed0ec144cdb68ad211436aa838
Accession Number: edsdoj.f1db94ed0ec144cdb68ad211436aa838
Database: Directory of Open Access Journals
More Details
ISSN:12592498
18764401
DOI:10.1016/j.artres.2017.06.006
Published in:Artery Research
Language:English