Vascular effect of lead on rabbit aortic smooth muscle

Abstract

Several reports have demonstrated a positive link between lead exposure and hypertension (Navas et al., 2007 and Heydari et al., 2006). It has also been suggested that alterations in vascular reactivity is one of several mechanisms by which lead induces hypertension (Webb et al., 1981). There are conflicting reports concerning the effect of lead on vascular reactivity. Some authors have reported an increase (Silveira et al. 2010) or decrease (Fiorim et al., 2011) in vascular reactivity to phenylephrine after lead exposure.  The goal of the present study was to investigate and characterize, using pharmacological methods the in-vitro vascular effects of lead exposure on isolated rabbit aortic smooth muscle. Rabbit aortic rings were isolated and mounted between two L shaped stainless steel holders in a 20ml organ bath containing PSS. Isometric contractions were recorded on a grass model 79D four channel polygraph. Dose response to Phenylephrine (PE) was examined both in the absence (control, n=8) and following 20mins exposure to 10^-4M lead acetate (n=8) in normal PSS. Acetylcholine (Ach) relaxation following 10^-7M PE pre-contraction was also examined both in the absence (control, n=7) and following 20mins exposure to lead acetate (10^-4M, n=7). The results showed that lead acetate significantly increased vascular reactivity to PE in rabbit aortic rings (P<0.05). The results also showed that lead acetate significantly decreased the relaxation response induced by Ach after PE pre-contraction (P<0.05). The depressed relaxation response to acetylcholine following lead exposure suggests impairment of endothelium-derived relaxant factor (EDRF).  The present study reinforces the concept that the association between lead poisoning and hypertension is related, at least in part, to enhanced vasocontractile response to phenylephrine as well as attenuated endothelium-dependent relaxation