Stimulation of Alpha₁-Adrenergic Receptor Ameliorates Cellular Functions of Multiorgans beyond Vasomotion through PPARδ

Figure 4

The effect of midodrine on cardiac energetic protein levels, hemodynamic status, aortic eNOS, and AT1R expression in the SHR groups. (a) The cardiac protein levels of p-AMPK, PPARδ, PGC-1α, and angiotensin II AT1 receptor; succinate dehydrogenase (SDH) activity; and ATP levels in the midodrine-treated and other animal groups. (b) Systolic, diastolic, and mean blood pressure and heart rate in the spontaneously hypertensive rat (SHR) groups. Data are expressed as the from each group ( per group). vs. control; ^# vs. atenolol. The red, green, and blue lines indicate groups II, III, and IV, respectively. (c) The aortic protein levels of p-AMPK and PPARδ in the midodrine-treated and other SHRs. (d) A representative picture of the immunohistochemistry results for eNOS antibodies in endothelial cells and AT1R expression in medial smooth muscle layers in midodrine-treated and other SHRs. Original magnification is 200 x. Groups: I, midodrine-treated group; II, atenolol-treated group; III, untreated control group. Data are expressed as the from each group ( per group). eNOS: endothelial nitric oxide synthase; AT1R: angiotensin II AT1 receptor.

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