Premium
Cardiac responses to GLP‐1 receptor activation are impaired in the setting of metabolic syndrome (1078.7)
Author(s) -
Conteh Abass,
Goodwill Adam,
Noblet Jill,
Sassoon Daniel,
Tune Johnathan,
Mather Kieren
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.1078.7
Subject(s) - medicine , cardiology , blood pressure , stroke volume , heart rate , inotrope , endocrinology , cardiac output , agonist , receptor
This study investigated the cardiovascular effects of the glucagon‐like peptide‐1 (GLP‐1) receptor agonist Exendin‐4 in lean vs. obese hearts. Left ventricular pressure‐volume relations were obtained following 24 hr intravenous infusion of saline‐vehicle or Exendin‐4 (30 fmol/kg/min) in lean (69 ± 4 kg) and obese (105 ± 2 kg) Ossabaw swine with metabolic syndrome (MetS). Measurements were obtained at rest, following 30 min occlusion of the left circumflex coronary artery, and following 2 hours of reperfusion. Baseline coronary flow, heart rate, and stroke volume were not different between vehicle‐treated lean and MetS swine. Exendin‐4 had no effect on end diastolic volume or stroke volume in lean or MetS swine. However, cardiac output and blood pressure were significantly increased relative to end‐diastolic filling volumes by Exendin‐4 administration in lean swine (P<0.05). Load independent assessment of cardiac inotropy revealed that Exendin‐4 increased the slope of the end systolic pressure volume relationship (ESPVR) from 2.9 ± 2.7 to 10.6 ± 2.4 mmHg/ml (p<0.05) in lean swine during ischemia. In contrast, Exendin‐4 had no effect on the relationship between cardiac output, blood pressure and end‐diastolic volume or on the ESPVR in MetS swine. These findings indicate that the cardiac inotropic actions of GLP‐1 receptor activation following ischemia/reperfusion injury are abolished in the setting of the metabolic syndrome. Grant Funding Source : Supported by NIH HL117620; NIH HL117620‐S1