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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Lead, ouabain and an endogenous plasma inhibitor were all found to be potent inhibitors of purified hog cerebral cortex sodium-potassium-activated adenosine triphosphatase and potassium-stimulated p-nitrophenyl-phosphatase. 2. The kinetic characteristics of inhibition of both enzymes by lead and the endogenous plasma inhibitor differed in several respects. For sodium-potassium-activated adenosine triphosphatase, lead and the endogenous plasma inhibitor were non-competitive inhibitors with respect to potassium; lead was competitive with respect to sodium, whereas the endogenous plasma inhibitor had no effect; lead was competitive with respect to magnesium adenosine triphosphate, whereas the endogenous plasma inhibitor was uncompetitive. For potassium-activated p-nitrophenylphosphatase, both lead and the endogenous plasma inhibitor were competitive with respect to potassium; lead showed a mixed type of inhibition with respect to p-nitrophenylphosphate, whereas the endogenous plasma inhibitor was non-competitive. 3. Lead and the endogenous plasma inhibitor exhibited synergistic inhibitory activity on sodium-potassium-activated adenosine triphosphatase. 4. These results suggest that lead could play a contributory role in the pathogenesis of essential hypertension via an additive inhibition of vascular smooth muscle sodium-potassium-activated adenosine triphosphatase.
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PMID:Effects of lead and a low-molecular-weight endogenous plasma inhibitor on the kinetics of sodium-potassium-activated adenosine triphosphatase and potassium-activated p-nitrophenylphosphatase. 216 8

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

Three atmospheric pollutants are discussed: Sulfur dioxide (SO2) acts as irritant gas on upper airways, trachea and large bronchi. Bronchoconstriction by SO2 is enhanced during work. Dose-response correlation may be observed with SO2 concentrations and bronchial hyperreactivity. Deaths and morbidity rates of patients with COPD parallel peaks of SO2 concentration such as occurred in the 1956 London smog. The mechanisms involved seem to be the same in cross sectional as in long term SO2 effects on human airways. Ozone (O3) is a major irritant pollutant. O3 penetrates deeply into the small airways, kills the macrophages and promotes infections. As peroxide it ruptures the cell membranes and thus lipogenases arise. Neutrophil leukocytes are attracted and transit into the peribronchiolar tissue, an enrichment which may be stopped in hydroxy-urea treated dogs. A marked correlation is observed between peribronchiolar tissue neutrophilia and bronchial hyperreactivity. This may even be a new pathway in the physiopathology of bronchial asthma. Lead is a constituent of exhaust particles and is easily absorbed into the blood. As in the case of drinking-water lead or otherwise absorbed lead, blood lead levels may be markedly reduced by adequate preventive measures. Diastolic and systolic blood pressures correlate significantly with the blood lead level. A further decrease would lower the incidence of myocardial infarctions, strokes and essential hypertension.
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PMID:[Air burden and respiratory and vascular diseases]. 389 59

Lead is a ubiquitous toxin, known to have adverse effects on the body even at low levels of exposure. In this review we explore whether low lead may be the principal or a major contributory cause of essential hypertension, and whether removal of lead from the environment may eventually reduce both the overall incidence of hypertension and the increased incidence with aging.
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PMID:Is lead exposure the principal cause of essential hypertension? 1220 46