Effects of Chronic Exposure to Mercury on Angiotensin-Converting Enzyme Activity and Oxidative Stress in Normotensive and Hypertensive Rats

Abstract

Background Mercury's deleterious effects are associated with increased cardiovascular risk. Objective To determine whether chronic exposure to inorganic mercury increases the activity of angiotensin-converting enzyme and its relationship with oxidative stress in several organs and tissues. Methods We studied male Wistar and spontaneously hypertensive rats (SHR) (3-month-old) exposed or not to HgCl 2 for 30 days. At the end of treatment, we investigated the following: changes in body weight, hemodynamic parameters, angiotensin-converting enzyme (ACE) activity and oxidative stress in the heart, aorta, lung, brain and kidney in hypertensive compared to normotensive animals. A value of p < 0.05 was considered significant. Results Chronic exposure to HgCl 2 did not affect weight gain in either group. Systolic blood pressure, measured weekly, did not increase in Wistar rats but showed a small increase in SHR rats. We also observed increases in left ventricular end-diastolic pressure and ACE activity in the plasma and hearts of normotensive rats. In the SHR+Hg group, ACE activity increased in plasma but decreased in kidney, lung, heart, brain and aorta. Oxidative stress was assessed indirectly by malondialdehyde (MDA) production, which increased in Hg-treated rats in both plasma and heart. In the SHR+Hg group, MDA increased in heart and aorta and decreased in lungs and brain. Conclusion These results suggest that chronic exposure to inorganic mercury aggravates hypertension and produces more expressive changes in ACE activity and oxidative stress in SHRs. Such exposure affects the cardiovascular system, representing a risk factor for the development of cardiovascular disorders in normotensive rats and worsening of pre-existing risks for hypertension.

The FAAH Inhibitor URB597 Modulates Lipid Mediators in the Brain of Rats with Spontaneous Hypertension

“…Hypertension is associated with redox imbalance that has previously been observed in the blood of patients with hypertension, as well as in the blood, heart, lungs, kidneys, and brain of rats with spontaneous hypertension [ 10 , 11 , 34 , 35 , 36 ]. At 20% of total O 2 consumption in the body, the high metabolic rate of the brain and the content of free iron ions promote the excessive production of ROS.…”

“…These phospholipids additionally make the brain vulnerable to oxidative modifications and, consequently, to metabolic disorders [ 8 ]. To-date, other studies have shown the presence of oxidative lipid and protein modification products in the brain of SHRs [ 35 , 36 ]. Thus, hypertension, which is accompanied by redox imbalance in the brain, may not only be a major risk factor for cerebrovascular problems such as stroke and cerebral hemorrhage, but may also promote the development of several neurological disorders (e.g., Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, amyotrophic lateral disease, and cerebellar ataxia) [ 38 ].…”

Oxidative stress-induced by 30 days of mercury exposure triggers acceleration of hypertension development in prehypertensive young SHR rats

“…In the SHR model in animals with previously established hypertension, we demonstrate that ACE activity levels increase with exposure to mercury. 50 However, before establishing hypertension in SHRs the metal exposure caused the opposite effect, a reduction in this enzyme activity. Mercury exposure accelerated the increase of SBP in SHR although the percentage of the losartan effect was reduced and ACE activity was also reduced in this exposed group.…”

Impact of Lipid Profile, Cardiac Biomarkers, Serum Angiotensin-Converting Enzyme Activity, Oxidative Stress and Antioxidant on Blood Pressure Status

“…MDA, a nal product of lipid peroxidation, is the most commonly measured biomarker of oxidative stress [32]. The increase in ACE activity could lead to increased activity of nicotinamide adenine dinucleotide phosphate oxidase [33,34] [40]. NO prevents platelet aggregation and activation of several cells (particularly monocytes, which are transformed into macrophages containing lipids) and inhibits proliferation of smooth muscle cells, which are integral components of atherosclerotic vascular lesions and stimulants of ROS and oxidative stress.…”