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

Figure 3

The effect of midodrine on energetic proteins, α₁-adrenergic receptor, UCP3, cytochrome c oxidase, GLUT4, succinate dehydrogenase activity, and ATP concentration in skeletal muscle tissues from SHRs. (a) Midodrine affected the expression of PPARδ, P-AMPKα, PGC-1α, α₁-adrenergic receptor, and UCP3. (b) Representative examples of immunohistochemical staining for GLUT4 and cytochrome c oxidase in skeletal muscle tissue slides from spontaneously hypertensive rats (SHRs) treated with midodrine or atenolol. Magnification is 200x. Groups: I, midodrine-treated group; II, atenolol-treated group; III, untreated control group. Data are expressed as the from each group ( per group). (c) Succinate dehydrogenase (SDH) activity in skeletal muscle from SHRs treated with midodrine or atenolol (estimated by a color reaction at 550 nm) and the ATP concentration in skeletal muscle estimated using an enzyme-linked immunosorbent assay.

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