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

Exposure to lead has been well recognized in a number of work environments, but little is known about lead exposure associated with machining brass keys containing lead. The brass that is widely used for key manufacturing usually contains 1.5% - 2.5 % of lead. Six (6) licensed locksmiths and 6 case-matched controls successfully completed the pilot study to assess the prevalence of increased body lead burden of professional locksmiths. We measured both Blood Lead (atomic absorption spectrometry), bone-lead (KXRF) and had each subject complete a health and lead exposure risk questionnaire. One locksmith had not cut keys during the past two years, therefore this subject and case-matched control was excluded from the blood lead analysis only. The average blood-lead concentration (+/-SEM) for the 5 paired subjects was 3.1 (+/- 0.4) microg/dL and 2.2 (+/- 0.3) microg/dL for controls. Bone measurements, including all 6 paired subjects, showed tibia lead concentration (+/-SEM) for locksmiths and controls was 27.8 (+/- 2.3) microg/g and 13.7 (+/- 3.3) microg/g, respectively; average calcaneus lead concentration for locksmiths and controls was 31.9 (+/- 3.7) microg/g and 22.6 (+/- 4.1) microg/g, respectively: The t-test shows a significantly higher tibia lead (p<0.05) and blood lead (p<0.05) for locksmiths than for their matched controls, but no significant difference for calcaneus lead (p>0.10). Given that the mean tibia bone lead concentration was 13.1 microg/g higher in locksmiths than in their matched controls, this average difference in the two groups would translate to an OR of increased hypertension in locksmiths of between 1.1 and 2.3, based on the published literature. Even with the very small number of subjects participating in this pilot study, we were able to demonstrate that locksmiths had significantly higher current exposure to lead (blood lead concentration) and significantly higher past exposure to lead (tibia lead concentration) than their age, sex and ethnically matched controls. Additional research is needed to fully identify the prevalence and associated risk factors for occupational exposure of lead in this previously understudied profession.
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PMID:Assessment of lead exposure risk in locksmiths. 1670 14

Chronic kidney disease (CKD) represents a major global public health concern. Efforts to prevent and/or slow progression of CKD are essential. Lead nephropathy, characterized by chronic tubulointerstitial nephritis, is a well-known risk of chronic, high-level lead exposure. However, in recent years, lead exposure has declined sharply, particularly in developed countries. We reviewed epidemiologic research in general, occupational, and patient populations to assess whether lead, at current exposure levels, still contributes to nephrotoxicity. Other pertinent topics, such as risk in children, genetic susceptibility, and co-exposure to cadmium, are also considered. The data reviewed indicate that lead contributes to nephrotoxicity, even at blood lead levels below 5 microg/dl. This is particularly true in susceptible populations, such as those with hypertension (HTN), diabetes, and/or CKD. Low socioeconomic status is a risk factor for both lead exposure and diseases that increase susceptibility. Future public health risk for lead-related nephrotoxicity may be most significant in those rapidly developing countries where risk factors for CKD, including obesity and secondary HTN and diabetes mellitus, are increasing more rapidly than lead exposure is declining. Global efforts to reduce lead exposure remain important. Research is also needed to determine whether specific therapies, such as chelation, are beneficial in susceptible populations.
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PMID:Lead-related nephrotoxicity: a review of the epidemiologic evidence. 1706 79

Lead (Pb(2+)) exposure is related to increased blood pressure or hypertension of human or animals. Abnormal vascular relaxant responses of low level Pb(2+) exposed animals were reported by several studies. However, it is difficult to tell whether these effects were induced directly by Pb(2+) or not. In this study we hypothesized that Pb(2+) can directly affect the relaxation of vessels. Male Wistar rat aortae were removed and cultured in PMRI 1640 with 1 ppm Pb(2+) (4.8 microM lead acetate) for 0.5, 6, 12 and 24h, and then their responses to acetylcholine (ACh) and sodium nitroprusside (SNP) were examined. After incubated for 24h, the relaxation induced by ACh was significantly decreased in Pb(2+) exposed aortic rings. However, there was not significant difference in relaxation induced by SNP between Pb(2+) exposed and control group. The nitrite in the culture media of aortic rings cultured for 24h, measured with Griess method, was significantly decreased in the Pb(2+) exposed group. The expression of endothelial NOS (eNOS) and isoform NOS (iNOS) in the homogenate of aortic rings cultured for 24h was measured by Western blot. The expression of eNOS of the Pb(2+) exposed group was significantly upregulated compared with that of the control group. However, there was no significant difference in the expression of iNOS in control and Pb(2+) exposed group. In conclusion, Pb(2+) was able to directly affect the relaxation of rat aorta. This effect may have some relation with the lower level of NO in the media, though the expression of eNOS was upregulated.
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PMID:Direct effects of lead (Pb2+) on the relaxation of in vitro cultured rat aorta to acetylcholine. 1740 86

Lead continues to pose a serious threat to the health of many children as well as adults. Concern about lead exposure as a significant public health problem has increased as evidence has mounted regarding adverse health effects at successively lower levels. This issue is complicated by the fact that there is no demonstrated biological function of lead in human. Lead potentially induces oxidative stress and evidence is accumulating to support the role of oxidative stress in the pathophysiology of lead toxicity. Lead is capable of inducing oxidative damage to brain, heart, kidneys, and reproductive organs. The mechanisms for lead-induced oxidative stress include the effects of lead on membranes, DNA, and antioxidant defense systems of cells. Recent epidemiological and toxicological studies have reported that lead exposure causes several diseases including hypertension, kidney disease, neurodegenerative disease and cognitive impairment. Although all these diseases include components of oxidative stress, the relevance of oxidative stress to lead-related diseases with low lead exposure has been criticized because most of the mechanistic studies have been conducted at moderate to higher dose levels. The association between low level lead exposure and oxidative stress has not been explored systematically. The present review focuses on mechanisms for lead-induced oxidative stress and relevance of oxidative stress to lead-related human disease with low lead exposure.
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PMID:Low level lead exposure and oxidative stress: current opinions. 1757 57

1. Lead is a common environmental and industrial toxin that can cause a variety of acute and chronic illnesses. For example, chronic exposure to low levels of lead has been shown to raise arterial pressure and promote renal and cardiovascular complications. 2. Several mechanisms have been identified by which chronic lead exposure can cause hypertension and cardiovascular disease. In recent years, increasing evidence has emerged pointing to the role of oxidative stress as a major mediator of lead-induced hypertension. 3. The present article provides an overview of the published studies on this subject.
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PMID:Interplay of reactive oxygen species and nitric oxide in the pathogenesis of experimental lead-induced hypertension. 1764 41

Low levels of chronic lead exposure can produce hypertension and endothelial dysfunction, which could be associated with oxidative stress, changes in vascular tone and an imbalance of endothelial-derived vasoconstriction and vasodilator factors. The aim was to investigate the effect of chronic lead-exposure on angiotensin II-induced vasoconstriction in isolated perfused kidney and microvessels. Male Wistar rats (230-250 g) were treated for 12 weeks with lead acetate (100 ppm, Pbgroup) or pure water (control group). We evaluated the vascular reactivity in the kidneys and renal microvessels in the presence and absence of N(omega)-nitro-L-arginine methyl ester (L-NAME) in both groups. The nitrite concentration in renal perfusate was measured as an index of NO released, renal abundance of 3-nitrotyrosine was measured as well as endothelial NO synthase (eNOS) expression. Oxidative stress was measured by using the oxidative fluorescence dye dihydroethidium (DHE) to evaluate in situ production of superoxide and identified by confocal microscopy. Lead-exposure significantly increased blood pressure, eNOS protein expression, oxidative stress and vascular reactivity to angiotensin II. L-NAME potentiated vascular response to angiotensin II in control group but had no effect on the Pb-group. Nitrites released from the kidney of lead-group was lower compared to the control group while 3-nitrotyrosine was higher. This data suggest that lead-induced hypertension could be caused partially by an altered NOsystem.
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PMID:Lead exposure effect on angiotensin II renal vasoconstriction. 1769 45

Lead is a potent environmental toxicant with well-known effects on intelligence, school achievement and behavior. Lead exposure is also associated with an increased risk of a variety of health problems including cancer, hypertension, cardiovascular disease, and renal disease. Considering the risk of hypertension, cardiovascular problems, and stroke following lead exposure, the current research assessed the extent to which postnatal exposure to environmentally relevant levels of lead could impair the recovery from a later occurring brain injury. Using a photochemical thrombotic stroke model we found that postnatal lead exposure significantly impaired post-stroke recovery of beam walking ability and proprioceptive limb placing. Considering the increased risk for hypertension and cardiovascular disease in lead-exposed humans, diminished capacity for repair or adaptation following lead exposure needs to now be examined in greater detail.
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PMID:Postnatal lead poisoning impairs behavioral recovery following brain damage. 1770 11

Chronic lead exposure has been epidemiologically linked with hypertension and renal disease. Clinical studies suggest that low lead levels may contribute to renal progression. However, experimental studies have not examined whether low levels of lead accelerate progression in experimental chronic renal disease. Sprague-Dawley rats were administered lead (L; 150 ppm in drinking water, n = 16) for 4 wk, followed by remnant kidney (RK) surgery with continuation of lead for an additional 12 wk; control rats (n = 9) were treated similarly but did not receive lead. Lead treatment was well tolerated and resulted in modest elevations in whole blood lead levels (26.4 +/- 4.5 vs. 1 +/- 0 mug/dl, week 16, P < 0.001). Lead treatment was associated with higher systolic blood pressure (P < 0.05) and worse renal function (creatinine clearance 1.4 +/- 0.4 vs. 1.8 +/- 0.5 ml/min, RK+L vs. RK, P < 0.05), and with a tendency for greater proteinuria (6.6 +/- 6.1 vs. 3.6 +/- 1.5 mg protein/mg creatinine, RK+L vs. RK, P = 0.08). While glomerulosclerosis tended to be worse in lead-treated rats (37.6 +/- 11 vs. 28.8 +/- 2.3%, RK+L vs. RK, P = 0.06), the most striking finding was the development of worse arteriolar disease (P < 0.05), peritubular capillary loss (P < 0.05), tubulointerstitial damage, and macrophage infiltration (P < 0.05) in association with significantly increased renal expression of monocyte chemoattractant protein-1 mRNA. In conclusion, lead accelerates chronic renal disease, primarily by raising blood pressure and accelerating microvascular and tubulointerstitial injury.
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PMID:Lead, at low levels, accelerates arteriolopathy and tubulointerstitial injury in chronic kidney disease. 1771 63

Following a hypertension symposium in Los Angeles in October 2007, a panel was convened to discuss how to treat hypertension in patients with coronary artery disease or with evidence of multiple major risk factors for coronary heart disease. Marvin Moser, MD, Clinical Professor of Medicine at the Yale University School of Medicine, New Haven, CT, moderated the discussion. Jackson T. Wright Jr, MD, PhD, Professor of Medicine, Program Director of William T. Dahms Clinical Research, and Director of the Clinical Hypertension Program at Case Western Reserve University, Cleveland, OH; Ronald G. Victor, MD, Professor and Division Chief, Hypertension, University of Texas Southwestern Medical Center, Dallas, TX; and Joel Handler, MD, Hypertension Lead, Care Management Institute, Kaiser Permanente, Anaheim, CA, participated in the discussion.
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PMID:How to treat hypertension in patients with coronary heart disease disease. 1845 99

Lead is a ubiquitous environmental toxin that is capable of causing numerous acute and chronic illnesses. Population studies have demonstrated a link between lead exposure and subsequent development of hypertension (HTN) and cardiovascular disease. In vivo and in vitro studies have shown that chronic lead exposure causes HTN and cardiovascular disease by promoting oxidative stress, limiting nitric oxide availability, impairing nitric oxide signaling, augmenting adrenergic activity, increasing endothelin production, altering the renin-angiotensin system, raising vasoconstrictor prostaglandins, lowering vasodilator prostaglandins, promoting inflammation, disturbing vascular smooth muscle Ca(2+) signaling, diminishing endothelium-dependent vasorelaxation, and modifying the vascular response to vasoactive agonists. Moreover, lead has been shown to cause endothelial injury, impede endothelial repair, inhibit angiogenesis, reduce endothelial cell growth, suppress proteoglycan production, stimulate vascular smooth muscle cell proliferation and phenotypic transformation, reduce tissue plasminogen activator, and raise plasminogen activator inhibitor-1 production. Via these and other actions, lead exposure causes HTN and promotes arteriosclerosis, atherosclerosis, thrombosis, and cardiovascular disease. In conclusion, studies performed in experimental animals, isolated tissues, and cultured cells have provided compelling evidence that chronic exposure to low levels of lead can cause HTN, endothelial injury/dysfunction, arteriosclerosis, and cardiovascular disease. More importantly, these studies have elucidated the cellular and molecular mechanisms of lead's action on cardiovascular/renal systems, a task that is impossible to accomplish using clinical and epidemiological investigations alone.
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PMID:Mechanisms of lead-induced hypertension and cardiovascular disease. 1856 11


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