Cardiac chronotropic competence to beta‐adrenergic stimulation in insulin resistance
Abstract only Insulin resistance (IR) precedes clinical manifestation of diseases such as diabetes mellitus and hypertension and is associated with increased sympathetic modulation. However, in the dexamethasone‐induced IR no changes have been noted in heart rate (HR). Therefore, we evaluated the he...
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Published in: | The FASEB journal Vol. 31; no. S1 |
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Main Authors: | , , , , , , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
01-04-2017
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Online Access: | Get full text |
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Summary: | Abstract only Insulin resistance (IR) precedes clinical manifestation of diseases such as diabetes mellitus and hypertension and is associated with increased sympathetic modulation. However, in the dexamethasone‐induced IR no changes have been noted in heart rate (HR). Therefore, we evaluated the heart chronotropic competence through beta‐adrenergic agonist stimulation in dexamethasone‐induced IR. Young male rats were divided into two groups: Control (CT)(n=6) and IR (n=6). CT and IR groups received vehicle or dexamethasone (DEX) (2mg/kg/day) i.p during seven days, respectively. To confirm Insulin resistance, insulin tolerance test (ITT) was performed after 6h fasted. Left femoral artery and vein were cannulated to measure blood pressure (2 kHz sampling rate) and isoproterenol (4μg/kg) administration respectively, 24h before evaluation. IR group presented attenuated decrease in glycaemia during ITT (CT: 42.5 ± 5 vs IR: 110.7 ± 14), hypertension (CT: 100 ± 2 vs IR: 135 ± 9 mmHg) without heart rate changes. In addition, increased cardiac sympathetic modulation by spectral analysis (LF/HF ratio CT: 0.52 ± 0.03 vs IR: 0.69 ± 0.04 un). After beta‐adrenergic stimulation IR group showed lower variation from basal level (ΔHR CT: 179 ± 4 vs IR: 78 ± 5 bpm). The reduction in heart chronotropic competence observed in this IR model could be a defense mechanism due cardiac sympathetic over activity.
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Fapitec‐SE; CAPES; CNPq. |
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ISSN: | 0892-6638 1530-6860 |
DOI: | 10.1096/fasebj.31.1_supplement.883.4 |