Alice V Araújo, Marcella D Grando, Roberto S DA Silva and Lusiane M Bendhack
The present study aimed to evaluate the K+ channels activation in vascular relaxation induced by the nitric oxide (NO) donors ruthenium-derived complex (Terpy) and sodium nitroprusside (SNP), as well as its protein expression, on mesenteric resistance arteries (MRA) isolated from renal hypertensive rats (2K-1C) and sham-operated rats (Sham). The NO donors Terpy and SNP induced relaxation with similar efficacy in isolated MRA from both 2K-1C and Sham rats, although SNP was more potent than Terpy. The maximum relaxation induced by Terpy was decreased when the voltagegated potassium channels were blocked in MRA from Sham, but not in 2K-1C rat arteries. The blockade of ATP-sensitive (KATP), big and small conductance Ca2+-activated (SKCa) or inward rectifier (KIR) potassium channels decreased the maximum relaxation induced by Terpy in MRA from Sham and 2K-1C rats. However, the maximum relaxation induced by SNP was inhibited in Sham but not in 2K-1C rats when the big conductance calcium-activated potassium channel was blocked. However, it remained the same when the other potassium channels were blocked. The protein expression of the SKCa and KATP were not altered in 2K-1C hypertensive rat MRA whereas the expression of KV and BKCa were augmented in MRA from 2K-1C rats. Therefore, the potassium channels play different role on the relaxation induced by SNP and Terpy. The activation of different potassium channels and the protein expression of potassium channels may be differently modulated in arteries from 2K-1C hypertensive rats when compared to normotensive rats.
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Journal of Hypertension: Open Access received 614 citations as per Google Scholar report
