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. 2020 May 13;11:402. doi: 10.3389/fphys.2020.00402

FIGURE 2.

FIGURE 2

β-Adrenergic signaling drives the cardiac phenotype in SAH, but not the vascular phenotype. (A) Bisoprolol (Bis; twice daily for 2 days with i.p. injections; 10 mg/kg initial pre-operative dose followed by 5 mg/kg for all subsequent injections) prevents the compromised cardiac function observed at 2-days post-SAH induction (sham n = 12, SAH n = 11, SAH + Bis n = 10). (B) However, bisoprolol treatment does not prevent the augmentation of myogenic reactivity in cremaster skeletal muscle resistance arteries isolated from SAH mice, nor (C) does it alter vasoconstriction in response to phenylephrine (sham diamax: 80 ± 2 μm, n = 13; SAH diamax: 80 ± 2 μm, n = 10; SAH + Bis diamax: 76 ± 2 μm, n = 7). (D) In naïve mice, the β-adrenergic receptor agonist isoproterenol (150 mg/kg i.p. for 2 days) reduces cardiac output (control n = 5, Isoproterenol n = 9). However, in contrast to SAH, both (E) myogenic reactivity and (F) phenylephrine responses in cremaster skeletal muscle resistance arteries isolated from isoproterenol-treated mice are attenuated (control diamax: 80 ± 4 μm, n = 8; isoproterenol diamax: 79 ± 2 μm, n = 8). *P < 0.05.