Nitric Oxide Donor Dilates Aorta in Salt Loaded Rats via Activation of Inward-Rectifier Potassium Channels
Since the mechanism of salt impairing NO-induced vascular relaxation is not fully clear, this study was designed to investigate the role of potassium (K+) channels in the vasodilatory effects of NO donor in salt loaded rats. Isolated thoracic aortic rings of adult male albino rats fed 8% NaCl containing diet for six weeks were used for isometric tension recording using PowerLab tissue bath system. The recorded data revealed that high salt diet (HS) did not change the relaxation responses to sodium nitroprusside (SNP, an NO donor) in rat's thoracic aortic rings. SNP-induced relaxation in salt loaded rats was significantly lower in rings contracted by high K+ than phenylephrine (PE, a selective α1-adrenergic receptor agonist). On the other hand, incubation of aortic rings from salt loaded rats with inward-rectifier K+ (KIR) channel blockers either individually or simultaneously with other K+ channel blockers significantly inhibited SNP-induced relaxation in PE-contracted rings; however incubation of rings with either calcium (Ca+2)-activated K+ (KCa), ATP-dependent (KATP) or voltage-sensitive K+ (KV) channels blockers had non-significant effects on relaxation responses of SNP. These results reveal that NO donor-induced aortic relaxation from salt loaded rats is mainly mediated by the activation of KIR channels.
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