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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The results of numerous epidemiological and experimental studies show that environmental exposure to lead in humans, as well as small doses of this element given to experimental animals exert hypertensinogenic and athoregenic effect. The vascular endothelium, involved in the development of arterial hypertension and arteriosclerosis, is now regarded as the main target organ for the toxic effect of lead. This metal can influence endothelium in various ways. Functional disturbances, mainly in respect of synthesizing and modifying functions of intravascular coagulation processes, impairment of endothelium integrity and cytotoxic effect have been observed. The lead-induced vascular damage may involve the inhibition of the repair processes of endothelial cells damaged by various exo- and endogenous factors. In addition, lead can also affect, directly or indirectly, the vasoactive function of endothelium through the increased production of reactive oxygen species. This effect of lead results in modified nitric oxide or endothelin synthesis and/or their release. Lead also accelerates the proliferation of smooth muscle cells and disturbs the synthesis of prostacyclins.
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PMID:[Lead effect on vascular endothelium]. 1273 10

Lead exposure is a known cause of hypertension. Although most studies have focused on lead-induced endothelial dysfunction and on the involvement of reactive oxygen species (ROS), it has been recently demonstrated that the vascular wall of lead-exposed rats has both an altered the endothelium-independent relaxing response and a reduced expression of soluble guanylate cyclase (sGC). The aim of the present study was to determine in in vitro incubated rat isolated aortic segments if lead downregulates sGC expression, analyzing the involvement of ROS and cyclooxygenase-2 (COX-2). The experiments were performed in isolated aortic segments from Wistar rats that were incubated with lead for 24 h. Lead significantly reduced sGC-beta(1) subunit expression in a concentration-dependent manner. The maximal reduction in sGC-beta(1) subunit expression was achieved with 1 ppm lead. Vitamin C (30 micromol/L) partially restored sGC-beta( 1) subunit expression in lead (1 ppm)-exposed aortic segments. A similar protection of sGC-beta(1) subunit expression was obtained with both a protein kinase A inhibitor, H89 (1 micromol/L) and with rofecoxib (1 micromol/L), an inhibitor of COX-2 activity. Moreover, lead exposure increased COX-2 expression in the arterial wall. While vitamin C reduced both COX-2 expression and superoxide anion production related to lead exposure, rofecoxib failed to modify superoxide anion generation in lead-incubated aortic segments. In conclusion, the present results suggest the involvement of ROS and COX-2 in the downexpression of sGC-beta(1) subunit induced by lead in the rat vascular wall.
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PMID:Lead-induced downregulation of soluble guanylate cyclase in isolated rat aortic segments mediated by reactive oxygen species and cyclooxygenase-2. 1276 Dec 46

Lead is a health hazard for all humans. Especially children under the age of six are most at risk for lead poisoning. Lead toxicity causes hematological, gastrointestinal, and neurological dysfunction. Symptoms are usually noted with blood lead greater than 2 micromoles/L. Severe or prolonged exposure may also cause chronic nephropathy, hypertension, and reproductive impairment. Lead inhibits some enzymes, alters cellular calcium metabolism, stimulates synthesis of binding proteins in kidney, brain, and bone, and slows down nerve conduction. Acute lead poisoning is relatively infrequent and results from ingestion of acid soluble lead compounds or inhalation of lead vapors but chronic exposure to low levels of the metal is still a public health issue, especially among some minorities and socioeconomically disadvantaged groups. Lead has been used since prehistoric times, and has become widely distributed and mobilized in the environment. Exposure to and uptake of this non-essential element have consequently increased. Both occupational and environmental exposures to lead remain a serious problem in many developing and industrializing countries and a public health problem of global dimensions.
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PMID:Inorganic lead toxicology. 1292 3

The National Committee for Quality Assurances (NCQA's) annual assessment of healthcare quality noted some good news and some bad news for the healthcare community. For the good news, more health plans and providers are approaching optimal results for several measures related to cardiovascular care and cancer prevention. However, failure of all plans to deliver the right preventive or follow-up care for other common conditions--such as diabetes and high blood pressure--means that more than 57,000 Americans are dying unnecessarily every year, NCQA estimated.
Qual Lett Healthc Lead 2003 Nov
PMID:Variations in quality causing needless deaths, new annual NCQA report says. 1467

Lead exposure adversely affects intellectual development in young children and might increase the risk for hypertension in adults. In the District of Columbia (DC), of an estimated 130,000 residences, approximately 23,000 (18%) have lead service pipes (Daniel Lucey, MD, DC Department of Health [DCDOH], personal communication, March 24, 2004). The Environmental Protection Agency (EPA) requires water authorities to test tap water in 10-100 residences annually for lead. In March 2003, DC Water and Sewer Authority (WASA) expanded its lead-in-water testing program to homes with lead service pipes extending from the water main to the house. By late January 2004, results of the expanded water testing indicated that the majority of homes tested had water lead levels above EPA's action level of 15 parts per billion (ppb). On February 16, DCDOH requested CDC assistance to assess health effects of elevated lead levels in residential tap water. DCDOH also requested deployment of officers of the United States Public Health Service (USPHS) to assist in the investigations. This report summarizes the results of the preliminary investigations, which indicated that the elevated water lead levels might have contributed to a small increase in blood lead levels (BLLs). The investigation of elevated water lead levels is ongoing. In the interim, DCDOH has recommended that young children and pregnant and breast-feeding women refrain from drinking unfiltered tap water.
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PMID:Blood lead levels in residents of homes with elevated lead in tap water--District of Columbia, 2004. 1505 94

Arsenicosis is a serious environmental chemical disease in China mainly caused by drinking water from pump wells contaminated by high levels of arsenic. Chronic exposure of humans to high concentrations of arsenic in drinking water is associated with skin lesions, peripheral vascular disease, hypertension, blackfoot disease, and high risk of cancers. Lead by the Ministry of Health of China, we carried out a research about arsenicosis in China recently. Areas contaminated with arsenic from drinking water are determined by 10% pump well water sample method while areas from burning coal are determined by existing data. Two epidemic areas of Shanxi Province and Inner Mongolia are investigated for the distribution of pump wells containing high arsenic. Well water in all the investigated villages of Shanxi Province showed polluted by high arsenic, and the average rate of unsafe pump well water is 52%. In Inner Mongolia, the high percentage of pump wells containing elevated arsenic is found only in a few villages. The average rate of unsafe pump well water is 11%. From our research, we find that new endemic areas are continuously emerging in China. Up to now, epidemic areas of arsenicosis mainly involve eight provinces and 37 counties in China. In the affected areas, the discovery of wells and coal with high levels of arsenic is continuing sporadically, and a similar scattered distribution pattern of patients is also being observed.
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PMID:Arsenic contamination and arsenicosis in China. 1527 5

In this prospective study, we examined changes in renal function during 6 years of follow-up in relation to baseline lead levels, diabetes, and hypertension among 448 middle-age and elderly men, a subsample of the Normative Aging Study. Lead levels were generally low at baseline, with mean blood lead, patella lead, and tibia lead values of 6.5 microg/dL, 32.4 microg/g, and 21.5 microg/g, respectively. Six percent and 26% of subjects had diabetes and hypertension at baseline, respectively. In multivariate-adjusted regression analyses, longitudinal increases in serum creatinine (SCr) were associated with higher baseline lead levels but these associations were not statistically significant. However, we observed significant interactions of blood lead and tibia lead with diabetes in predicting annual change in SCr. For example, increasing the tibia lead level from the midpoints of the lowest to the highest quartiles (9-34 microg/g) was associated with an increase in the rate of rise in SCr that was 17.6-fold greater in diabetics than in nondiabetics (1.08 mg/dL/10 years vs. 0.062 mg/dL/10 years; p < 0.01). We also observed significant interactions of blood lead and tibia lead with diabetes in relation to baseline SCr levels (tibia lead only) and follow-up SCr levels. A significant interaction of tibia lead with hypertensive status in predicting annual change in SCr was also observed. We conclude that longitudinal decline of renal function among middle-age and elderly individuals appears to depend on both long-term lead stores and circulating lead, with an effect that is most pronounced among diabetics and hypertensives, subjects who likely represent particularly susceptible groups.
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PMID:Lead, diabetes, hypertension, and renal function: the normative aging study. 1528 63

Previous studies from this laboratory have demonstrated the presence of oxidative stress and its role in the pathogenesis of lead-induced hypertension. This study was designed to determine whether oxidative stress in animals with lead-induced hypertension is associated with dysregulation of the activities of the main antioxidant enzymes, namely superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPX). In addition, we aimed to determine the effect of lead on the regulation of guanylate cyclase (GC) expression. Male Sprague-Dawley rats were randomly assigned to control and lead-exposed groups, and immunodetectable Cu/Zn SOD, Mn SOD, CAT, and GPX were determined by immunoblotting in the thoracic aorta. Additionally, the activities of these enzymes were measured in the renal cortex, medulla, and thoracic aorta. Furthermore, immunodetectable GC was determined in the thoracic aorta. In the thoracic aorta, lead exposure resulted in significant upregulation of aortic Cu/Zn SOD activity, while CAT and GPX activity and CuZn SOD, Mn SOD, and CAT protein abundance were unchanged. Conversely, GC protein abundance was decreased in thoracic aorta. In renal cortex and medulla, CAT and Cu/Zn SOD activities were increased, while GPX activity was unchanged. Lead-exposed animals exhibited upregulation of some antioxidant enzyme activities, most likely as a compensatory response to lead exposure. However, other enzymes did not compensate in the face of oxidative stress, suggestive of an antioxidant/oxidant imbalance. These findings, combined with decrease in aortic GC protein abundance, provide further evidence for dysregulation of antioxidant/oxidant balance and hypertension in this model.
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PMID:Lead-induced dysregulation of superoxide dismutases, catalase, glutathione peroxidase, and guanylate cyclase. 1572 81

Lead is a metal widely spread in the natural environment. It is strongly toxic, particularly to the peripheral and central nervous systems. The toxic influence on the cardiovascular system is most pronounced in case of higher exposures, where myocardium and the renal circulation are affected, in consequence of which secondary arterial hypertension can develop. It seems that lead affects the cardiovascular system mainly by changing the peripheral autonomic nervous system and leading to chronic neuropathy. Chronic exposure, even to low doses of lead, can impair conduction in myocardium. In order to assess those changes thoroughly prospective studies involving newly employed workers with occupational exposure to toxic activity of lead will be necessary.
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PMID:[Effect of lead on the cardiovascular system]. 1575 46

This case-control study was designed to examine the association between blood lead levels and high blood pressure in a restricted subpopulation, Saudi women who were 45-93-year old, during or after menopausal period and not occupationally exposed to lead. Blood lead levels were assessed in 100 women with hypertension and 85 control subjects. Lead concentrations were measured in the whole blood using flameless atomic absorption spectrophotometry. Blood pressure measurements were performed according to the World Health Organization recommendations. Results revealed that the mean blood lead levels for hypertensive were 47.52+/-39.26 and 45.59+/-28.55 microg/l for controls. Participants were classified according to the median of blood lead levels in order to compute odds ratios. After controlling a number of potential confounding variables, the multiple logistic regression analysis revealed that women with blood lead levels of > or = 38.6 microg/l were 5.27 times more likely to be hypertensive than those with blood lead levels of < 38.6 microg/l, but of borderline significance (p = 0.06). Although such observation might support the hypothesis that the depletion of lead from bones during menopause increases blood lead levels placing women at increased risk for high blood pressure, there is a need for further studies with larger number of subjects. A number of risk factors, which were suspected to influence blood lead levels, were also investigated. Use of Kohl, duration of its use, osteoporosis disease and intake of calcium supplements were significantly associated with blood lead levels.
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PMID:Is lead considered as a risk factor for high blood pressure during menopause period among Saudi women? 1621 19


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