Abstract
The participation of ROS production and nucleotides signaling in the TH‐induced vasodilation was investigated. T3 was added to VSMC primary culture or administered to rats to evaluate the expression of Nox1 and 4, P2Y1,2, and 6. Redox status was assessed by the measurement of glutathiones (Arbor Assays, MI, USA). Results show that T3 (10−8 M, 24 h) increased Nox1 protein and Nox4 mRNA expression in VSMC (n=3). Besides, the expression of P2Y1, 2 and 6 mRNA seem to be decreased in T3‐treated VSMC (10−8 and 10−7 M, 24 h). Experimental hyperthyroidism was confirmed by increased cardiac mass (heart weight (mg)/tibia's length (mm): 33.17 ± 3.34, n=15 vs 27.49 ± 2.24, n=14 in control, p<0.05) and non‐detectable levels of total T4. Nox4 protein expression is increased in T3‐treated animals (7 μg/100 g body weight, i.p., 14 days), n=4. Moreover, oxidized glutathione (GSSG) is significantly diminished in hyperthyroid animals (4.15 ± 0.60, n=8 vs 1.98 ± 0.30, n=9 in control group, p<0.05) while the ratio reduced (GSH)/oxidized glutathione is significantly higher in T3 group (6.71 ± 1.4, n=8 vs 15.64 ± 3.5 in control animals, n=9, p<0.05), suggesting a more preserved antioxidant status in these animals. The present data disclose the participation of ROS production and purinergic signaling in the TH‐induced vasodilation.
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