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Figure 3 | Cardiovascular Diabetology

Figure 3

From: Impaired relaxation despite upregulated calcium-handling protein atrial myocardium from type 2 diabetic patients with preserved ejection fraction

Figure 3

Myocardial function during β-adrenergic stimulation. In response to incrementing doses of β-adrenergic agonist dobutamine (10-7 to 10-5 M) right atrial cardiac muscles from non-diabetic patients (non-DM, closed circles, n = 8) showed an increase in amplitude of contraction (Fdev, A), and speed of contraction (+dF/dtmax, B); and a faster speed of early relaxation (-dF/dtmin, C) and late relaxation (Tau, D). Strikingly, both the increase in the contractile parameters (Fdev and + dF/dtmax) and the hastening of the relaxation parameters (-dF/dtmin and Tau) were absent in the cardiac muscles from the diabetic patients (DM, open circles, n = 6). E. Western blotting was performed with human cardiac tissue samples from non-diabetic (non-DM) and diabetic (DM) patients probed for β1–adrenoceptor (β1-AR) and β-actin. In representative blot β1–AR was detected just below 50 kDa and β-actin above 37 kDa as loading control. F. Western blot analysis showed similar protein expression for β1–adrenoceptor. For all functional parameters two-way ANOVA Bonferroni’s posthoc: dose effect, * = p < 0.05 and DM effect, # = p < 0.05). For protein analysis data obtained from four replica experiments, non-DM (n = 10) and DM (n = 9) patients, unpaired t-test. Data are mean ± SEM.

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