Volume 65, Issue 12 (2 2008)                   Tehran Univ Med J 2008, 65(12): 17-22 | Back to browse issues page

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Badalzadeh R, Norouzzadeh A, Asgari A, Khoshbaten A. Effects of low level of lead exposure on blood pressure and responsiveness of the rat isolated heart to adrenergics. Tehran Univ Med J. 2008; 65 (12) :17-22
URL: http://tumj.tums.ac.ir/article-1-682-en.html
Abstract:   (4050 Views)

Background: Exposure to low levels of lead increases blood pressure in humans and animals. Although there are controversial reports about the exact mechanisms of lead-induced hypertension, many factors such as alteration in the cardiovascular responsiveness to endogenous substances including catecholamines could be one of the mechanisms involved. In the present study, the effect of lead acetate on the systolic blood pressure and responsiveness to β-adrenergics was investigated in rats.

Methods: Through their drinking water, three groups of rats were exposed to 100 ppm lead acetate for periods of 4, 8 or 12 weeks. The blood pressures of the rats were monitored throughout the study. The rat hearts were isolated and perfused with Krebs-Henseleit solution (pH=7.4) at 37˚C and gassed with 95% O2 + 5% CO2. The heart rate (chronotropic) and contractile (inotropic) responses were recorded before and after adding isoproterenol at multiple concentrations to the perfusion solution.

Results: The mean blood pressures in the 8 and 12-week lead-treated groups were significantly higher than that of the control group (P<0.01). The chronotropic response to many doses of isoproterenol was significantly increased in the 12-week lead-treated group compared to that of the control group (P<0.05). The inotropic response to this drug was significantly increased in both the 8- and 12-week lead-treated rats (P<0.05 and P<0.01, respectively).

Conclusions: Our results indicate that low-levels of lead increase systolic blood pressure as well as both chronotropic and inotropic effects of β-adrenergics, which could imply an important role in the pathogenesis of lead-induced hypertension.

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