Lead can elevate blood Pressure

A current research conducted by Reza Badalzadeh, Ali Norouzzadeh, Azhdar Heydari, Alireza Asgari and Ali Khoshbaten
of Department of Physiology and Biophysics, Medical Faculty of Baqiyatallah University of Medical Sciences, Tehran and Research Center for Chemical Injuries (RCCI), Baqiyatallah University of Medical Sciences, Tehran, Iran has demonstrated the effect of Lead in elevating blood pressure in humans and causing associated health problems.

Introduction

Lead is a heavy metal that is distributed widely in our environment as a consequence of its increasing use in industries; Hence it appears commonly as a part of effluent in water bodies.Lead intoxication may cause neurological, hematological, gastrointestinal, and cardiovascular dysfunction in humans.In recent decades, the relationship between blood lead levels and blood pressure (BP) has been extensively investigated and chronic exposure to low levels of lead has been shown to cause hypertension in both humans and animals.

Effects of Lead
Other reported cardiovascular changes following lead exposure include alteration in ECG, impaired cardiac conduction, increased incidence of arrhythmias and alteration in the force of cardiac contraction (contractility). These findings were mainly derived from in vivo studies done on humans and in vitro experimental studies.

Hypertension may occur following any alteration in the function of the systems that regulate blood pressure; whether it be a change in stroke volume or cardiac rate or even reduction in vagal firing. The experimental findings suggest that lead acts at multiple sites within the cardiovascular, renal, and nervous systems.

Experimental Findings
Subchronic exposure to low levels of lead increases Heart Rate and cardiac contractility as well as arterial blood pressure. This level of exposure over periods of 8-12 weeks prolonged the ST interval without causing any significant alteration in QRS duration.

The incidence of arrhythmia and AV block increased the ST interval without any significant alteration being caused in QRS duration. The incidence of arrhythmia and AV block increased only after 12 weeks of exposure, but there were no significant changes in coronary flow. Following the increase of lead in plasma levels, the content of lead in the heart tissue (and other tissues) increases as well.

It was noted that Heart Rate (HR) increased dose-independently in lead-exposed rats and no certain relationship between tachycardia and duration of exposure was observed. The HR remains unchanged in the early phases of exposure to low levels of lead, with tachycardia occurring only in the late stages. As the lead content of the body increases, the HR tends to decline because of lead-induced abnormalities in the cardiac conduction system.

Pharmacology of Lead
Increased HR and contractility as well as arterial blood pressure in lead-exposed animals may be due to the ability of this metal to alter cellular metabolism of Calcium ions . Studies on Calcium ions and the vascular effects of lead have shown that intracellular Calcium -binding sites are involved in the action of this metal in vascular smooth muscle. A similar finding was reported in the case of the heart, as Calcium influx was observed in both atrial trabeculae and in the papillary muscles of the heart. The increase in Calcium influx and elevation of intracellular content of Calcium by lead may be due to the action of this metal in altering Calcium transport processes, such as activation of protein kinase C (that activates Calcium channel opening), inhibition of Sodium-Potassium- ATPase pump etc. The increased Heart Rate and cardiac contractility following the augmented intracellular Calcium concentrations causes hypertension due to increased cardiac output. Low levels of lead in the early phases of exposure were not able to alter the rhythm of the heart, as arrhythmogenesis and AV block were elicited only in the late phases of exposure (after 12 weeks). So, the toxic effects of long-term, low-level lead exposure on the cardiac conducting system are more likely to be a chronic phenomenon. Moreover, the decreased cardiac contractile function observed following chronic exposure to higher levels of lead may be attributable to the cardiac conduction defects which occur in that condition. Beside the Calcium pathway, other factors may also be involved in mediating the action of lead, eg, nitric oxide (NO), catecholamines, endothelin, and the rennin-angiotensin system (RAS).

It has been found out that lead causes constriction of blood vessels through a direct effect on the endothelial cells and thus reduces blood flow. It may be that lead tends to reduce coronary flow (by mechanisms such as inhibition of nitric oxide synthesis or increased release of endothelin (which consequently causes vasodilatation) or rennin-angiotensin system activation). Following lead-induced increase in cardiac work, a metabolic vasodilatation occurs in coronary vessels and this factor actually prevents any coronary flow reduction

Conclusion
The present findings demonstrate that subchronic exposure to low levels of lead induces an increase in HR and cardiac contractility as well as in arterial blood pressure.While, no certain relationship was observed between tachycardia and duration of lead exposure. Cardiac conduction defects are less likely to occur in the early phases of exposure to low levels of lead: it seems to be the result of chronic exposure.

Renference Link: http://www.ijp-online.com/article.asp?issn=0253-7613;year=2008;volume=40...