Abstract
Lead (Pb) exposure causes hazardous effects as hypertension and other cardiovascular diseases. We evaluated whether chronic Pb exposure alters the peripheral vascular resistance measuring the vascular reactivity of mesenteric resistance arteries in rats to identify the underlying mechanisms that are associated to the development of Pb-induced hypertension. Mesenteric resistance arteries from lead-treated and untreated Wistar rats (1st dose: 10 μg/100 g; subsequent doses: 0.125 μg/100 g, intramuscular, 30 days) were used. Contractile responses to phenylephrine increased, while acetylcholine and sodium nitroprusside-induced relaxation was not affected by lead treatment. Endothelium removal and inhibition of NO synthase by L-NAME similarly enhanced the response to phenylephrine in untreated and lead-treated rats. The antioxidants apocynin and superoxide dismutase (SOD) did not affect vasoconstriction in either group. The vascular expression of cyclooxygenase-2 (COX-2) protein increased after lead exposure. The respective non-specific or specific COX-2 inhibitors indomethacin and NS398 reduced more strongly the response to phenylephrine in treated rats. Antagonists of EP1 (SC19220), TP (SQ29548), IP (CAY10441) and angiotensin II type 1 (losartan) receptors reduced vasoconstriction only in treated rats. These conclusions present further evidence that lead, even in small concentration, produces cardiovascular hazards being an environmental contaminant that account for lead-induced hypertension.
Highlights
Lead is an environmental and industrial pollutant without a biological role
This study investigates the role of oxidative stress, COX-2 and its derived prostanoids, and angiotensin II in the vascular reactivity changes in mesenteric resistance arteries induced by 30-day treatment with a low lead concentration
The Ach-induced vasodilator responses (Rmax, Ct: 97,78 ± 0.86 n = 10, Pb: 98.73 ± 0.61% n = 12; EC50, Ct: −7.78 ± 0.38 n = 10, Pb −8.07 ± 0.06, n = 12) and SNP (Rmax, Ct: 77.13 ± 3.57 n = 5, Pb: 73.31 ± 3.47% n = 4; EC50, Ct: −5.78 ± 0.3 n = 5, Pb: −6.19 ± 2.23 n = 4) were unaffected by lead treatment (Figures 1B,C), suggesting that the metal did not affect the endothelial function of the mesenteric rings
Summary
Lead is an environmental and industrial pollutant without a biological role. It exerts toxic effects on several organs and systems of the organism, including the development of hypertension (Xie et al, 1998). Several reports suggest that it contributes to the genesis and/or maintenance of hypertension increasing hemodynamic parameters and peripheral vascular resistance. Lead Increase Vascular Peripheral Resistance as increased sympathetic activity and renin-angiotensin system and insulin resistance are involved in humans (Freis, 1973; Harrap, 1994). Only recently the role of toxic metals has aroused the curiosity of the scientific world in the genesis of hypertension (for reviews see Prozialeck et al, 2008; Vassallo et al, 2011; Shakir et al, 2017)
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
