Vascular Effect of Lead on Rabbit Aortic Smooth Muscle

Abstract

Several reports have demonstrated a positive link between lead exposure and hypertension. It has also been suggested that 
alterations in vascular reactivity is one of several mechanisms by which lead induces hypertension. There are conflicting reports 
concerning the effect of lead on vascular reactivity. Some authors have reported an increase or decrease 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 precontraction (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.