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

Chronic lead exposure resulting in blood lead concentrations that exceed 1.93 mumol/l (40 micrograms/dl) or chelatable urinary lead excretion greater than 3.14 mumol (650 micrograms) per 72 h has been associated with renal disease. A previous study had found greater chelatable urine lead excretion in subjects with hypertension and renal failure than in controls with renal failure due to other causes, although mean blood lead concentrations averaged 0.92 mumol/l (19 micrograms/dl). To determine if chelatable urinary lead, blood lead, or the hematologic effect of lead (zinc protoporphyrin) were greater in hypertensive nephropathy (when hypertension precedes elevation of serum creatinine) than in other forms of mild renal failure, we compared 40 study subjects with hypertensive nephropathy to 24 controls having a similar degree of renal dysfunction due to causes other than hypertension. Lead burdens were similar in both the study and control groups as assessed by 72-h chelatable urinary lead excretion after intramuscular injection of calcium disodium EDTA (0.74 +/- 0.63 vs. 0.61 +/- 0.40 mumol per 72 h, respectively), and by blood lead (0.35 +/- 0.23 vs. 0.35 +/- 0.20 mumol/l). We conclude that subjects from a general population with hypertensive nephropathy do not have greater body burdens of lead than renal failure controls.
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PMID:Body burdens of lead in hypertensive nephropathy. 251 Jun 13

Clinical and experimental studies suggest an association between low-level lead exposure and hypertension. This association was investigated in six 3-month-old dogs who were randomly paired with their littermates. The daily oral dose of lead acetate was 1.0 mg Pb/kg body wt for 5 months; the controls received equimolar sodium acetate. Blood pressure was measured indirectly without anesthesia and was similar in the two groups at the start of the study. The mean blood pressure was higher in the lead-exposed group at every follow-up, from 10 days to 20 weeks. This treatment group difference in profiles was statistically significant (repeated-measures ANOVA, p = 0.0048). The final mean blood pressures were 120 +/- 6.4 (x +/- SE) vs 108 +/- 1.5 mm Hg. At 4 weeks the plasma renin activity was higher in the lead-exposed group: 3.4 +/- 0.25 vs 1.2 +/- 0.15 ng/ml/hr. The difference decreased during the study but the elevated trend persisted (repeated-measures ANOVA, p = 0.014). Lead exposure did not alter renal functions or extracellular fluid volume. This study shows that low-level lead intake in young dogs can cause an early increase in blood pressure which persists during ongoing exposure and which is associated with a small increase in the activity of the renin-angiotensin system.
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PMID:Blood pressure elevation in young dogs during low-level lead poisoning. 328 20

Lead is a common element in the earth's crust, serving useful purposes in industry, but serving no purpose in the human body. Increase in blood pressure is an important public health problem with numerous factors contributing to many facets of the disease. The relationship of lead exposure and increased blood pressure has long been considered, but only recently critically investigated. Reports of subtle changes in calcium metabolism and renal function, as well as in vitro studies examining end-arteriolar smooth muscle contractility, link lead exposure and increased blood pressure. This paper critically examines the evidence associating chronic low-level lead exposure and increased blood pressure. The review focuses on epidemiological, clinical, and toxicological data. The epidemiological evidence is consistent with low-level exposure to lead causing an elevation in blood pressure. The strength of that association, and the dose-response characteristics, are less certain. Individual resistance and susceptibility could affect the degree of blood pressure elevation. The results of animal and in vitro studies are consistent with the epidemiological evidence, and suggest biologically plausible mechanisms for the association. The most probable mechanisms are intracellular perturbations in calcium metabolism mediated by direct lead effects at the end-arteriole, and indirect effects via renal dysfunction. Better indices of lead exposure and lead activity are needed to quantify these effects in humans. New and safer methods of chelating lead suggest interesting approaches for studying the relationship between lead and hypertension. This link could have significant implications in determining what constitutes a 'safe' level of environmental lead exposure, and whether a proportion of essential hypertension could be 'cured' by chelation therapy.
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PMID:Chronic low-level lead exposure. Its role in the pathogenesis of hypertension. 329 24

Lead intoxication was recognised as early as 2000 BC and the widespread use of lead has been a cause of endemic chronic plumbism in several societies throughout history. In the twentieth century, lead intoxication is still a common problem. In children it is largely due to ingestion of pica and environmental exposure, whereas adult groups at greatest risk are the industrially exposed: thus, screening of these workers should be undertaken at regular intervals. The clinical features of lead intoxication are nonspecific and often go unrecognised. The early manifestations are largely neuropsychiatric, followed by more significant disturbances of the central and peripheral nervous systems, symptomatic gastrointestinal, musculoskeletal, haematological and endocrine abnormalities. The association of lead poisoning with renal disease is well documented and must be considered, particularly if there is associated hypertension and/or gout. Blood lead concentrations are an unreliable predictor of body lead stores as they are indicative only of recent exposure. Haematological parameters have been used to assess those at risk of toxicity, but although more reliable than blood concentrations, they also fail to predict those patients at risk of toxicity. The recommended assessment for patients with suspected lead intoxication is a calcium disodium edetate chelation test, which is a sensitive marker for assessing body stores and subsequent intoxication. In children the dosage should be 50 mg/kg up to 1000 mg, and in adults 1000 mg administered intravenously or 2000 mg intramuscularly in divided doses 12 hours apart with subsequent 72 hour urinary lead estimations. Lead excretion levels greater than 350 micrograms/72 hours should be considered as suggestive of intoxication, particularly if supported by historical, clinical or biochemical evidence of lead exposure. Treatment of patients with positive chelation tests involves symptomatic treatment and a course of chelation therapy utilising calcium disodium edetate in doses similar to those used for testing, and in the more severely intoxicated patient, the addition of dimercaprol in doses of 75 mg/m2 every 4 hours to a total of 300 mg/m2/day. The safety of these treatment regimens is well documented.
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PMID:Lead intoxication. 354 May 17

Pregnancy hypertension, blood pressure during labor, and the umbilical cord blood lead concentration were assessed in 3851 women for whom additional demographic, medical, and personal information was available. Lead levels correlated with both systolic (Pearson r = 0.081, p = 0.0001) and diastolic (r = 0.051, p = 0.002) blood pressures during labor. The incidence of pregnancy hypertension increased with lead level. Multivariate models of pregnancy hypertension and systolic blood pressure as a function of maternal age, parity, hematocrit, ponderal index, race, and diabetes were improved by including lead as a predictor variable. At these observed levels of exposure (mean blood lead, 6.9 +/- 3.3 [SD] micrograms/dl), lead appears to have a small but demonstrable association with pregnancy hypertension and blood pressure at the time of delivery, but not with preeclampsia.
Hypertension 1987 Oct
PMID:Pregnancy hypertension, blood pressure during labor, and blood lead levels. 365 74

Lead MC5 bipolar exercise ECG was obtained in 510 asymptomatic males, aged 40 to 65, utilizing the bicycle ergometer, with maximal stress in 71% of the subjects. "Ischemic changes" occurred in 61 subjects, the frequency increasing from 4% at age 40 to 45, to 20% at age 50 to 55, to 37% at age 61 to 65. Subjects having an ischemic type ECG change on exercise had more frequent minor resting ECG changes, more resting hypertension, and a greater incidence of high cholesterol values than subjects with a normal ECG response to exercise, but there was no difference in the incidence of obesity, low fitness, or high systolic blood pressure after exercise. Current evidence suggests that asymptomatic male subjects with an abnormal exercise ECG develop clinical coronary heart disease from 2.5 to over 30 times more frequently than those with a normal exercise ECG.
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PMID:The maximal exercise ECG in asymptomatic men. 501 28

Exposure to lead in early life may result in chronic renal disease in adulthood. To test this hypothesis, we gave Sprague-Dawley rats, from 3 to 9 weeks of age, either tap water or a 1% lead acetate solution, and we studied them (in pairs) 3 and 16 weeks after exposure; that is, at 12 and 25 weeks of age. Lead-intoxicated animals failed to grow. Their GFR's were lower compared with the matched controls and fell between 12 and 25 weeks of age from 4.8 +/- 0.3 to 3.3 +/- 0.4 ml/min/g dry kidney wt (P less than 0.01). Changes in RBF and single nephron GFR were proportional to changes in total kidney GFR, indicating that superficial and deep nephrons were equally affected. The blood pressure in the lead-exposed animals studied at 25 weeks of age was 143.2 +/- 3.7 mm Hg, a value significantly higher than that of 130.4 +/- 3.3 observed in controls (P less than 0.05). These results demonstrate that limited exposure to lead during development can result in progressive renal insufficiency and hypertension.
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PMID:Lead intoxication during development: its late effects on kidney function and blood pressure. 739 18

Thirty-two male veterans participated in a study to determine cumulative lead exposure in an urban population. Subjects were chosen on the basis of blood pressure status in order to attempt to compare lead exposure between patients with and without hypertension. Patients currently enrolled in hypertension clinic and on treatment were recruited and matched with controls for age, race, and socioeconomic status. Each subject underwent provocative chelation via slow intravenous infusion of CaNa2 EDTA and 6-h urinary lead measurement and completed an interviewer-administered questionnaire. Twenty blacks and 12 whites participated, with a median age of 52 years (range: 27 to 72). Urinary lead excretion ranged from below detection limits to frankly toxic levels in an individual with heavy moonshine ingestion. Lead levels were higher than reported in other non-workplace populations. The distribution of lead values was skewed, as expected, with a median excretion of 75 mcg lead/6 h (corresponding to a median 24 degrees post-chelation urinary lead excretion of 286 mcg) and modal values between 50 and 75 micrograms lead. Levels of 95 mcg lead/6 h (corresponding to 24 degrees levels of 333 mcg lead) and above were considered "high" (N = 11) and the remainder were "low" (N = 21). Among those able to recall various characteristics of their first childhood dwellings, the presence of flaking paint in a multiple family dwelling was strongly associated with "high" lead excretion (X2 = 9.32, p = 0.009). Hypertensives excreted slightly more lead than nonhypertensives, although the difference was not statistically significant in this small sample. Lead excretion was not associated with current (treated) blood pressure determinations among hypertensives. However, lead excretion was associated with systolic pressure as recorded on entry to the hypertension clinic (N = 21, R2 = 0.24, p = 0.03).
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PMID:Predictors of lead stores in male veterans. 747 75

Environmental lead (Pb2+) contributes a small but significant risk to human hypertension. It is postulated that the hypertensinogenic action of Pb2+ may be due, in part, to its direct action on vascular smooth muscle cells. To investigate this hypothesis, freshly isolated rat aortic smooth muscle (RASM) cells were propagated in defined media containing one of two Centers for Disease Control-based concentrations of Pb2+ (as lead citrate): 100 and 500 micrograms Pb2+/l (i.e., equivalent to 5.5 and 27.5 micrograms Pb2+/dl blood; designated 100-RASM and 500-RASM). Control (CON-RASM) cells received sodium citrate. 500-RASM cells exhibited suppressed propagation and fell out of propagation synchrony with CON-RASM cells: when CON-RASM cell approached confluence (approximately 90%), 500-RASM cell density was 6.4% that of CON-RASM cell density. By contrast, 100-RASM cells exhibited marked hyperplasia albeit this was not apparent until passage 3 (p3). Overall, when p3-p6 CON-RASM cells approached confluence, 100-RASM cell density was 107.6% greater than CON-RASM cell density. The protein content of CON-RASM and 100-RASM was not different, whereas that of 500-RASM cells was 29% greater than that of CON-RASM and 100-RASM cells. Phase-contrast microscopy revealed that 100 micrograms Pb2+/l converted normal spindle-shaped/ribbon-shaped RASM cells into less spread, cobblestone-shaped, neointimal-like cells. Immunocytochemical analysis revealed that 100-RASM cells lacked or had markedly fewer actin cables, characteristic of rapidly dividing cells. In addition, Pb(2+)-treated RASM cells exhibited altered membrane fatty acyl composition with a trend towards an increase (by as much as 50%) in membrane arachidonic acid. Interestingly, hyperplastic 100-RASM cells exhibited a 70.6% reduction in angiotensin II (Ang II) receptor concentration whereas the concentrations of alpha 1- and beta-adrenergic and atrial natriuretic peptide (ANP) receptors were not affected. In addition, in experiments designed to control for Pb(2+)-associated differences in RASM cell propagation, there was a concentration-dependent decrease in Ang II receptor concentration: for 100 and 500 micrograms Pb2+/l, Ang II receptor concentration was decreased 39.6% and 65.5%, respectively. Thus, although Pb2+, depending on its concentration, had contrasting effects on RASM cell propagation, it had a consistent, concentration-dependent inhibitory effect on Ang II receptor concentration. Recovery (r) from Pb2+ required at least two additional passages. At p71r the enhanced propagation (+54%) and reduced Ang II receptor concentration (-49%) of 100r-RASM cells persisted.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Lead alters growth and reduces angiotensin II receptor density of rat aortic smooth muscle cells. 756 89

The effect of elevated blood lead levels on the blood pressure of children has not been clearly described. In order to define this association better, we conducted a cross-sectional study, evaluating the association between lead and high blood pressure. Using a Dinamap monitor to measure blood pressures, blood pressures and blood lead levels were measured in 149 children (ages 1-10 years) receiving medical care at the General Medical and Lead Poisoning Clinics at Children's Hospital of Philadelphia. Blood lead levels ranged from 7 to 70 mg/dL with a mean of 27 mg/dL. The mean systolic blood pressure was 108 mmHg and the mean diastolic reading was 63 mmHg. Higher systolic blood pressure was significantly correlated with increased weight, age, and height. Diastolic pressure was significantly associated with weight and height. There was a small, negative correlation between blood lead levels and systolic blood pressure, and a positive but insignificant correlation between lead levels and diastolic blood pressure. Our study population had both higher mean lead levels and a higher prevalence of hypertension than is true of the U.S. population as a whole. We concluded that elevated blood lead levels are not associated with elevated blood pressure in children.
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PMID:The effect of blood lead on blood pressure in children. 818 78


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