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

Cadmium is a highly toxic element that is cumulative and has a long biological half-life in mammals. The severe toxicity of cadmium in man has been known for more than 100 years. Despite the knowledge that cadmium is toxic, only 20 human cases of poisoning via ingestion were recorded prior to 1941, whereas in the ensuing five-year period more than 680 cases of cadmium poisonings from accidental oral ingestion of this metal were documented. Some of the recorded effects of exposure to cadmium in laboratory animals include renal tubular damage, placental and testicular necrosis, structural and functional liver damage, osteomalacia, testicular tumors, teratogenic malformations, anemia, hypertension, pulmonary edema, chronic pulmonary emphysema, and induced deficiencies of iron, copper, and zinc. Some of these effects have also been observed in human after accidental exposures to cadmium oxide fumes and are characteristic of the syndrome described in Japan as Itai Itai disease in which ingestion of cadmium is the inciting chemical.
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PMID:Cadmium inhalation and male reproductive toxicity. 240 89

A case-control study was performed to assess whether cadmium is related to hypertension in a non-occupationally exposed population. 63 male subjects affected by mild stable hypertension, pharmacologically untreated, were investigated together with 63 male normotensive controls individually matched for sex, age, body mass index, smoking habits and work activities. Cadmium in blood, zinc and copper in serum, the three elements in urine and hair, together with some biological parameters involved in pathogenesis of hypertension, were investigated. The mean Cd blood value in hypertensives (H) was 0.58 micrograms/L vs 0.44 micrograms/L in normotensives (N) (t = 2.03; p less than 0.05) with a greater difference in non-smokers (0.41 micrograms/L vs 0.25 micrograms/L) (t = 2.69, p less than 0.01). Furthermore, both systolic and diastolic blood pressure were significantly related to cadmium blood levels (r = 0.20 and 0.19 respectively, p less than 0.05). Smoking habit affected cadmium levels only in the blood, not in the other biological matrices examined. No significant difference of cadmium content in urine and hair was found between normotensives and hypertensives but Cd/Cu ratio in urine was significantly lowered in the second group.
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PMID:Cadmium in blood, urine and hair related to human hypertension. 253 33

In our study we investigated 36 out-patients with renal disease, 22 of whom were hypertensive. In all patients proteinuria was present (4.30 +/- 5.05 g protein/day) and kidney diseases were verified by renal biopsy. Blood cadmium in non-smokers was significantly (p less than 0.05) lower than in smokers. We found a positive correlation between cadmium-concentration of blood and urine (p less than 0.01, R = 0.44) and between cadmium-concentration of blood and blood uric acid (p less than 0.01, R = 0.44). Proteinuria was weakly correlated with cadmium concentration of urine (p less than 0.05, R = 0.35). Patients with renal hypertension showed a significantly higher (p less than 0.05) urine cadmium excretion per day (1.60 +/- 1.12 micrograms/day) compared to normotensives with a disease of the kidney (1.14 +/- 1.47 micrograms/day). Our results indicate that cadmium may be involved in the development of hypertension in patients with renal disease.
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PMID:Does cadmium contribute to the development of renal parenchymal hypertension? 259 74

Exposure to lead results in accumulation in proximal renal tubular lining cells in the form of morphologically discernible inclusion bodies which are lead-protein complexes. Acute nephrotoxicity consists of proximal tubular dysfunction and can be reversed by treatment with chelating agents. Chronic lead nephrotoxicity consists of interstitial fibrosis and progressive nephron loss, azotaemia and renal failure. Potential complications of lead nephropathy include gout and hypertension. Cadmium accumulates in renal tubular lining cells bound to metallothionein, a small protein containing 30% cystine. Metallothionein protects against nephrotoxicity by binding cadmium in a nontoxic form. Renal tubular dysfunction and chronic interstitial fibrosis occur when cadmium levels in the renal cortex exceed the critical concentration of about 200 micrograms/g. Recommendations are made for specific research needs.
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PMID:Mechanisms of lead and cadmium nephrotoxicity. 265 22

The best definition of risk factors for renal injury, irrespective of the aetiological agent, comes from observations in patients with acute renal failure. From such observations, two subdivisions have evolved, i.e., acute insults and host risk factors. Acute renal insults include: hypertension, sepsis, use of nephrotoxic drugs (e.g., aminoglycoside antibiotics and contrast media), haemoglobinuria or myoglobinuria, liver disease and extracellular volume depletion. Host risk factors include: advanced age, hypertension, gout and hyperuricaemia, diabetes mellitus, chronic renal failure and use of diuretics. Furthermore, the mechanism of acute renal injury can be correlated with different risk factors: for a tubular toxic agent, acting either directly on the cells or haemodynamically, a dose-dependency is characteristic; while for immunologically mediated injury, genetic predisposition is more important. The identification of risk factors for chronic toxic injury is confounded by the possibilities of multiple episodes of subclinical renal injury, the distinct possibility that a major component of the ageing process may be a loss of renal reserve, and a progressive body burden, of, e.g., cadmium, which may deplete intrinsic protective mechanisms. However, clinically relevant risk factors can alert the clinician to exercise additional caution when prescribing medications that are potentially nephrotoxic. Such factors include dehydration, pre-existing renal disease, age, co-existing diseases that cause renal ischaemia, gender, concomitantly administered drugs, and electrolyte abnormalities.
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PMID:Risk factors for toxic nephropathies. 265 33

Cadmium exposure is known to induce hypertension, but development of hypertension is not universal in exposed animals. However, the cellular uptake of cadmium could also exert renal cytotoxic effects which have been, until now, essentially only studied at the proximal tubule level. Kallikrein is an enzyme synthetized in renal cortex and excreted in the urine in the distal tubule. Therefore, to evaluate the distal renal effect of cadmium, we studied the daily urinary kallikrein excretion (UKE) in conscious unrestrained female Brown Norway rats during long-term chronic exposure to 2 dosages of cadmium given subcutaneously 3 times a week, a low dose (LD): 0.25 mg/kg and a high dose (HD): 1 mg/kg. Neither dose of cadmium was able to induce significant hypertension in the treated animals. HD administration for 24 weeks resulted in a decreased UKE associated with an increase in plasma renin activity and sodium and potassium excretions. LD administration had no significant effect on UKE. Twenty weeks after stopping cadmium administration, a persistent reduction in UKE was still observed; furthermore, the group which had been previously administered a LD of cadmium, now also exhibited a reduced UKE. During this re-examination period in both groups, the UKE reductions were associated with normal systolic blood pressure, glycosuria, natriuresis. Our data show that cadmium administration can influence UKE, plasma renin activity, plasma aldosterone concentration and electrolyte excretion without inducing any variation of blood pressure. This may reflect a nephrotoxic, non-hypertensive effect. Since this effect persisted after stopping cadmium administration, it may indicate a prolonged irreversible nephrotoxic effect at the distal nephron level. Thus, UKE may be a useful non-invasive index to evaluate distal nephrotoxicity.
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PMID:Renal kallikrein excretion as a distal nephrotoxicity marker during cadmium exposure in rats. 265 77

In our study we investigated 36 patients with renal disease, 22 of whom were hypertensive. In all proteinuria was present (4.30 +/- 5.05 g protein/day) and renal lesions were proved by renal biopsy. Blood cadmium in non-smokers was significantly (P less than 0.05) lower than in smokers. We found a positive correlation between cadmium concentrations in blood and urine (P less than 0.01, r = 0.44) and between cadmium concentration in blood and serum uric acid levels (P less than 0.01, r = 0.44). Proteinuria was weakly correlated with cadmium concentration in urine (P less than 0.05, r = 0.35). Patients with hypertension showed a significantly higher (P less than 0.05) urine cadmium excretion per day (1.60 +/- 1.12 micrograms/day compared with normotensives with disease of the kidney (1.14 +/- 1.47 micrograms/day). Our results indicate that cadmium may be involved in the development of hypertension in patients with renal disease.
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PMID:Cadmium and renal hypertension. 272 70

Chronic cadmium chloride (CdCl2, 0.5 and 1.0 mg/kg, i.p.) treatment in female albino rats for 2 weeks resulted in elevation of blood pressure. In chronic CdCl2-treated rats the pressor responses to different doses of noradrenaline, angiotensin II and depressor responses to acetylcholine and isoprenaline were unaltered. In rat hindquarter preparation there was elevation of perfusion pressure and the sensitivity of vascular bed to noradrenaline was increased in the CdCl2-induced hypertensive rats. Complete bilateral adrenalectomy or chemical sympathectomy or treatment with captopril did not prevent the development of CdCl2-induced hypertension. Treatment with verapamil (15 mg/kg/day, p.o.) or nifedipine (10 mg/kg/day, p.o.) for 2 weeks prevented the development of hypertension with chronic CdCl2 treatment. It is suggested that chronic treatment of rats with CdCl2 induces hypertension. It is possible that cadmium mimics the calcium ion for the induction of hypertension in rats.
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PMID:Cadmium-induced hypertension in rats. 275 62

In developed countries, hypertension represents one of the most frequent diseases and is one of the most important risk factors of arteriosclerotic vascular disease e.g. to myocardial infarction or cerebral apoplexy. The etiology of hypertension is unknown in about 90% of cases. The heavy metals cadmium and lead occur in increasing amounts in the human environment. Numerous epidemiological studies and investigations using experimental animals have dealt with the putative relationship between cadmium and lead, and hypertension. The results to date have been quite controversial; thus the issue appears to be unresolved at present. In the present study scalp hair samples were collected from 100 non-smoking 30-to-50-year-old men. After washing, the samples were digested with a mixture of nitric and sulfuric acid in a teflon bomb and analyzed by flameless atomic absorption spectroscopy. For 90% of the test persons the cadmium hair values were in the range of 0 to 1400 micrograms/kg; the corresponding range for hair lead was 0 to 13,000 micrograms/kg. Correlation with diastolic or systolic blood pressure was neither found for cadmium or lead. The test persons with the highest cadmium or lead load were not hypertensive. Some factors should be considered when comparing the present results with those of other investigators reporting a positive correlation in the question under consideration. 1. Previous studies in man frequently did not sufficiently take smoking habits into account. This is essential, however, because, in addition to cadmium and lead, nicotine and carbon monoxide are also constituents of tobacco smoke and contribute to an increase in blood pressure. 2. Previous investigations generally employed blood samples, which is disadvantageous in comparison with the analysis of hair because blood samples do not reflect long-term exposition, which is important in the etiology of chronic diseases. Correlation between hypertension and levels of long-term cadmium and lead exposure in man seem to be unlikely in light of the present results. Nevertheless, numerous potential effects should be considered to obtain further insight in the complex pathogenesis of hypertension.
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PMID:[Correlation of blood pressure and cadmium and lead content of the hair in nonsmoking males]. 275 43

In our study we investigated 36 out-patients with renal disease; 22 of them were hypertensive. In all patients proteinuria was present (4.30 +/- 0.82 g protein/d) and renal involvement has been proved by renal biopsy. Blood cadmium in nonsmokers was significantly (P less than .05) lower than in smokers. Patients with renal hypertension showed a significantly higher (P less than .05) urine cadmium excretion/d (1.60 +/- 0.23 micrograms/d) compared to normotensives with a disease of the kidney (1.14 +/- 0.38 micrograms/d). Our results indicate that cadmium may be involved in the development of hypertension in patients with renal disease.
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PMID:Role of cadmium in hypertensive patients with renal parenchymal disease. 275 5


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