Activation of K+ Channels and Na+, K+ ATPase Prevents Aortic Endothelial Dysfunction in 7 Day Lead‐treated Rats

Abstract

We previously demonstrated that exposure for 7 days with a low lead concentration increased systolic blood pressure (SBP) and nitric oxide bioavailability in aortic rings as a compensatory mechanism in the initial stage of lead exposure. We investigated if lead treatment also alters the participation of K+ channels and Na+, K+‐ATPase (NKA) on vascular function. Wistar rats were treated with lead (1st dose 4 μg/100 g, subsequent dose 0.05 μg/100 g, i.m. to cover daily loss) or vehicle. Lead treatment reduced contractile response of aortic rings to phenylephrine (PHE) but did not change vasodilator responses induced by acetylcholine (ACh) or sodium nitroprusside (SNP). Furthermore, lead exposure increased basal O2− production and apocynin, superoxide dismutase and catalase reduced the response to PHE only in treated animals. Lead treatment also increased aortic NKA functional activity. When aortic rings were precontracted with high KCl or preincubated with tetraetilamonium, 4 aminopyridine (4AP), iberiotoxin (IbTX), apamin and charybdotoxin the ACh‐induced relaxation was more reduced in treated animals. 4‐AP and IbTX also reduced more the relaxation elicited by SNP in treated animals. Results suggest that lead‐treatment promoted NKA activation as well as of K+ channels and this effect might contribute to preserve aortic endothelial function against increased SBP and oxidative stress. (CAPES, FAPES/CNPq)