Preliminary Studies of Acute Cadmium Administration Effects on the Calcium-Activated Potassium (SKCa and BKCa) Channels and Na+/K+-ATPase Activity in Isolated Aortic Rings of Rats

• Published in: Biological trace element research Vol. 183; no. 2; pp. 325 - 334
• Main Authors: Vassallo, Dalton V., Almenara, Camila C. P., Broseghini-Filho, Gilson Brás, Teixeira, Ariane Calazans, da Silva, David Chaves F., Angeli, Jhuli K., Padilha, Alessandra S.
• Format: Journal Article
• Language: English
• Published: New York Springer US 01.06.2018; Springer Nature B.V
• Subjects: Acetylcholine; Aorta; Bioavailability; Biochemistry; Biomedical and Life Sciences; Biotechnology; Cadmium; Calcium; Calcium channels; Calcium channels (voltage-gated); Calcium conductance; Calcium ions; Cardiovascular diseases; Channels; Electric potential; Endothelium; Epithelium; Heart diseases; Heavy metals; Incubation period; Life Sciences; Na+/K+-exchanging ATPase; Neurotransmitters; NG-Nitroarginine methyl ester; Nitric oxide; Nutrition; Oncology; Pollutants; Potassium; Potassium channels; Potassium channels (calcium-gated); Potassium channels (voltage-gated); Potassium conductance; Rats; Resistance; Stretching; Tetraethylammonium; Vasodilation; Verapamil; Cadmium; Na; Vascular reactivity; ATPase; K; Potassium channels; Heavy metal; Na+/K+-ATPase
• ISSN: 0163-4984; 1559-0720
• DOI: 10.1007/s12011-017-1150-8

Cadmium is an environmental pollutant closely linked with cardiovascular diseases that seems to involve endothelium dysfunction and reduced nitric oxide (NO) bioavailability. Knowing that NO causes dilatation through the activation of potassium channels and Na + /K + -ATPase, we aimed to determine whether acute cadmium administration (10 μM) alters the participation of K + channels, voltage-activated calcium channel, and Na + /K + -ATPase activity in vascular function of isolated aortic rings of rats. Cadmium did not modify the acetylcholine-induced relaxation. After L-NAME addition, the relaxation induced by acetylcholine was abolished in presence or absence of cadmium, suggesting that acutely, this metal did not change NO release. However, tetraethylammonium (a nonselective K + channels blocker) reduced acetylcholine-induced relaxation but this effect was lower in the preparations with cadmium, suggesting a decrease of K + channels function in acetylcholine response after cadmium incubation. Apamin (a selective blocker of small Ca 2+ -activated K + channels—SK Ca ), iberiotoxin (a selective blocker of large-conductance Ca 2+ -activated K + channels—BK Ca ), and verapamil (a blocker of calcium channel) reduced the endothelium-dependent relaxation only in the absence of cadmium. Finally, cadmium decreases Na + /K + -ATPase activity. Our results provide evidence that the cadmium acute incubation unaffected the calcium-activated potassium channels (SK Ca and BK Ca ) and voltage-calcium channels on the acetylcholine vasodilatation. In addition, acute cadmium incubation seems to reduce the Na + /K + -ATPase activity.