However, this reduction was much more marked in arteries obtained from lead-treated mTOR inhibitor rats. The residual relaxation to ACh in high-KCl precontracted vessels was abolished by L-NAME indicating an additional effect of NO, independent of K+ channel activation, on ACh-induced relaxation. TEA was initially used to evaluate the overall contribution of K+ channels to the basal tone and ACh-induced relaxation. TEA increased basal tone more in preparations from the lead-treated rats compared to the untreated rats and reduced the relaxation induced by ACh more in aortic segments from the lead-treated
than untreated group; these results suggest a greater contribution of K+ channels in both basal tone and ACh-induced relaxation after lead treatment. Accordingly, Fiorim et al.
(2011) observed that TEA potentiated the phenylephrine response more strongly in aortic rings from lead-treated rats compared to untreated rats. In addition, patch clamp observations of K+ currents in human erythrocytes showed that lead exposure activates K+ channels (Kempe et al., 2005). Different K+ channels are involved in cardiovascular disorders, such as atherosclerosis, hypertension and stroke (Nelson and Quayle, 1995, Callera et al., 2004 and Ledoux SB431542 order et al., 2006). Lead treatment increased NO bioavailability in the rat aorta (Fiorim et al., 2011) and as mentioned NO could open K+ channels. Therefore, we investigated the participation of diverse K+ channels in regulating basal tone and in NO-mediated ACh-induced relaxation in lead-treated second rats. It has been shown that aortic tone is strongly dependent on the activity of Kv channels (Tammaro et al., 2004). In addition, Cheong et al. (2002) also has shown the participation of Kv channel currents in small blood vessels. Our results showed that 4-aminopyridine, a selective inhibitor of Kv channel, induced a greater increase in basal tone in aortic segments from lead-treated than in untreated rats. Furthermore, this inhibitor reduced the relaxation induced by ACh to a greater extent in preparations
from lead-treated compared to untreated rats. These results suggest that Kv channels contribute to the regulation vascular tone in the rat aorta and that channels contribute more to the basal tone and ACh-induced relaxation in the lead-treated rats. Several studies have shown that BKCa plays a key role in regulating vascular tone in different beds (Cheong et al., 2002, Eichhorn and Dobrev, 2007 and Briones et al., 2009), and the activation of these channels is an important component of the EDHF response in several vascular beds (Ledoux et al., 2006). Our results show that both charybdotoxin (KCa and Kv blocker) and apamin (selective SKCa blocker) did not modify basal tone in aortic segments from both groups.