*2.8. Aortic Function*

Segments (2 mm) of the descending thoracic aorta were dissected free of fat and connective tissue in ice-cold PSS gassed with 95% O2 and 5% CO2 and set up on an isometric wire myograph (model 410 A; Danish Myo Technology, Aarhus, Denmark) filled with PSS (37 ◦C; 95% O2 and 5% CO2), as described [36]. The vessels were stretched to 6 mN and allowed to equilibrate for 45 min. Afterwards, aortas were contracted twice with 100 mM KCl, and after washing, vessels were left to equilibrate (30 min) before starting the experiments. Endothelial-dependent vasodilatations to acetylcholine (ACh; 10−<sup>9</sup> to 10−<sup>4</sup> M) and endothelial-independent vasodilatations to sodium nitroprusside (10−<sup>10</sup> to 10−<sup>3</sup> M) were performed in phenylephrine (Phe)-precontracted (70–100% of 100 mM KCl contraction) vessels. Contractile responses to the α1-adrenoceptors agonist Phe (10−<sup>9</sup> to <sup>3</sup> × <sup>10</sup>−<sup>4</sup> M) were also studied.
