Insulin-induced changes in ?-adrenergic response: An experimental study in the isolated rat papillary muscle

Ferrara, Nicola; Abete, Pasquale; Corbi, Graziamaria; Paolisso, Giuseppe; Longobardi, Giancarlo; Calabrese, Claudio; Cacciatore, Francesco; Scarpa, Donatella; Iaccarino, Guido; Trimarco, Bruno; Leosco, Dario; Rengo, Franco

doi:10.1016/j.amjhyper.2004.10.006

Cited by 20 publications

(16 citation statements)

References 26 publications

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“…Recent experimental results from our lab as well as others depicted a direct positive inotropic effect of insulin on both normal and simulated I/R cardiomyocytes [20,21]. However, existing data concerning the functional effects of insulin on the myocardial response to b-AR activation are quite limited and inconsistent [30][31][32].…”

Section: Discussionmentioning

confidence: 86%

Insulin inhibits β-adrenergic action in ischemic/reperfused heart: a novel mechanism of insulin in cardioprotection

Zhou

et al. 2007

Apoptosis

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Section: Discussionmentioning

confidence: 86%

Insulin inhibits β-adrenergic action in ischemic/reperfused heart: a novel mechanism of insulin in cardioprotection

Zhou

et al. 2007

Apoptosis

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“…[12][13][14] Insulin's inotropic effect may be related to enhanced ␤-adrenoreceptor sensitivity as well as improved calcium handling properties of the myocyte. 15,16 T3 acts on the myocyte directly and indirectly and by genomic and nongenomic mechanisms. 17,18 It is able to lower vascular resistance 7,19 and have positive effects on the adrenoreceptor and calcium handling properties of the myocyte.…”

Section: Discussionmentioning

confidence: 99%

Glucose-Insulin-Potassium and Tri-Iodothyronine Individually Improve Hemodynamic Performance and Are Associated With Reduced Troponin I Release After On-Pump Coronary Artery Bypass Grafting

et al. 2006

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Background— Both glucose-insulin-potassium (GIK) and tri-iodothyronine (T3) may improve cardiovascular performance after coronary artery surgery (CABG) but their effects have not been directly compared and the effects of combined treatment are unknown. Methods and Results— In 2 consecutive randomized double-blind placebo-controlled trials, in patients undergoing first time isolated on-pump CABG between January 2000 and September 2004, 440 patients were recruited and randomized to either placebo (5% dextrose) (n=160), GIK (40% dextrose, K + 100 mmol · L −1 , insulin 70 u · L −1 ) (0.75 mL · kg −1 h −1 ) (n=157), T3 (0.8 μg · kg −1 followed by 0.113 μg · kg −1 h −1 ) (n=63) or GIK+T3 (n=60). GIK/placebo therapy was administered from start of operation until 6 hours after removal of aortic cross-clamp (AXC) and T3/placebo was administered for a 6-hour period from removal of AXC. Serial hemodynamic measurements were taken up to 12 hours after removal of AXC and troponin I (cTnI) levels were assayed to 72 hours. Cardiac index (CI) was significantly increased in both the GIK and GIK/T3 group in the first 6 hours compared with placebo ( P <0.001 for both) and T3 therapy ( P =0.009 and 0.029, respectively). T3 therapy increased CI versus placebo between 6 and 12 hours after AXC removal ( P =0.01) but combination therapy did not. Release of cTnI was lower in all treatment groups at 6 and 12 hours after removal of AXC. Conclusions— Treatment with GIK, T3, and GIK/T3 improves hemodynamic performance and results in reduced cTnI release in patients undergoing on-pump CABG surgery. Combination therapy does not provide added hemodynamic effect.

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“…In addition, insulin might modulate the inotropic response of ␤-adrenergic receptor agonists in mammalian hearts. A low concentration of insulin (0.3 nmol/liter) sensitized the positive inotropy of isoproterenol in the isolated rat papillary muscle, 33 but a high concentration (6 mol/liter) impaired the inotropic effect of norepinephrine in cat papillary muscle. 10 Baltensperger et al 34 showed that insulin is able to stimulate insulin receptor-catalyzed phosphorylation of the ␤ 2 -adrenergic receptor.…”

Section: Discussionmentioning

confidence: 98%

Cellular Mechanisms Responsible for the Inotropic Action of Insulin on Failing Human Myocardium

Hsu

Wei

Chen

et al. 2006

The Journal of Heart and Lung Transplantation

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Insulin-induced changes in ?-adrenergic response: An experimental study in the isolated rat papillary muscle

Abstract: Our results suggest that the insulin-induced modulation of contractility is calcium independent and insulin leads to a supersensitization on the beta(1)-adrenoceptors without effects on beta-adrenoceptor independent adenylate cyclase-related pathway.

Cited by 20 publications

References 26 publications

Insulin inhibits β-adrenergic action in ischemic/reperfused heart: a novel mechanism of insulin in cardioprotection

Insulin inhibits β-adrenergic action in ischemic/reperfused heart: a novel mechanism of insulin in cardioprotection

Glucose-Insulin-Potassium and Tri-Iodothyronine Individually Improve Hemodynamic Performance and Are Associated With Reduced Troponin I Release After On-Pump Coronary Artery Bypass Grafting

Cellular Mechanisms Responsible for the Inotropic Action of Insulin on Failing Human Myocardium

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