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

Although most were unknown a few years ago, present evidence indicates that at least 25 trace elements have some pertinence to health. Unlike vitamins, they cannot be synthesized. Some trace elements are now considered important only because of their harmful effects but traces of them may be essential. Zinc is especially important during puberty, pregnancy and menopause and is related to protein metabolism. Both fluoride and cadmium accumulate in the body year after year. Cadmium is positively correlated with several chronic diseases, especially hypertension. It is obtained from smoking and drinking soft water. Silicon, generally associated with silicosis, may be necessary for healthy bone and connective tissue. Chromium, believed to be the glucose tolerance factor, is obtained from brewer's yeast, spices, and whole wheat products. Copper deficiency may be implicated in a wide range of cardiovascular and blood related disorders. Either marginal deficiencies or slight excesses of most trace elements are harmful. Nurses should instruct patients to avoid highly refined foods, fad diets, or synthetic and fabricated foods. A well balanced and varied diet is the best safeguard against trace element excesses or deficiencies.
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PMID:Trace elements: implications for nursing. 689 39

Glucose Tolerance Factor (GTF) is synthesized in vivo from absorbed dietary chromium, and acts as a physiological enhancer of insulin activity, binding to insulin and potentiating its action about three-fold. Since GTF is well absorbed orally, the development of sufficiently concentrated and stable supplementary sources of this agent may enable convenient and physiologically appropriate pharmacological modulation of insulin activity. A review of the numerous physiological actions of insulin suggests a number of therapeutic applications for GTF, in such diverse ailments as diabetes mellitus, hyperlipidemia, reactive hypoglycemia, obesity, cancer, protein malnutrition or malabsorption, endogenous depression, Parkinsonism, hypertension and cardiac arrhythmias. GTF supplementation may also have value in preventive medicine.
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PMID:The therapeutic potential of glucose tolerance factor. 700 27

The glomerular filtration rate (GFR) was determined in rats with an isogeneic kidney transplant and compared with that of unilaterally nephrectomized rats. Experiments were carried out in adult rats, 3 months of age, weighing approximately 300 g, as well as in juvenile rats, 6 to 8 weeks of age, weighing approximately 170 g. All donor kidneys were taken from adult rats. The GFR was measured regularly, using a chromium 51-EDTA clearance technique which permitted repeated measurements to be taken in the same animals, during a 15-week followup period. After unilateral nephrectomy the GFR per 100 g body weight (BW) increased compared with that of a single normal kidney. Adult transplant recipients had a GFR per 100 g BW of about 80% of that of unilaterally nephrectomized rats. There was no statistical difference in the GFR when comparing adult recipients of either a normal or a hyperfunctional kidney. When isografts were transplanted to juvenile recipients, there was an initial decrease in the absolute GFR compared with the donor value in the case of a normal adult donor kidney. This decrease was even more pronounced when a hyperfunctioning kidney was transplanted to a juvenile recipient. However, when related to BW the GFR was, as in the adult recipients, about 80% of that of unilaterally nephrectomized juvenile rats. During the followup period the systolic blood pressure was measured regularly by tail plethysmography, in order to detect any blood pressure elevations, which are a frequent complication in adult and pediatric human renal transplantation. However, no hypertension was observed after isogeneic kidney transplantation in the various groups. These results show that the GFR of isogeneically transplanted rat kidneys amounts to about 80% of the maximally attainable level. Isogeneic transplantation of an adult kidney to a juvenile recipient results in a rapid adaptation of the GFR to the smaller size of the body and does not cause an increase in blood pressure.
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PMID:The glomerular filtration rate of isogeneically transplanted rat kidneys. 704 95

The study was carried out in 24 male rats with spontaneous hypertension (SHR, Kyoto Wistar) and control Wistar rats aged 8 and 12 weeks with the objective of detecting the time of activation of large cell neurosecretory nuclei of the anterior hypothalamus in rats with spontaneous hypertension. The activity of neurons of the supraoptical and paraventricular nuclei was evaluated by two quantitative methods. One of them allows the study of distribution of neurosecretory cells by phases of synthesis in these nuclei in 8- and 12-week-old animals. Along with this morphometrical method, the average diameter of neurosecretory cells and their nuclei was determined after Gomori's staining with chromium-alumen hematoxylin. Spontaneously hypertensive and control normotensive rats by 12 weeks of development were found to have an enhanced function of neurosecretory nuclei apparently associated with the age change in their functional activity. In spontaneously hypertensive rats, more pronounced activation of the supraoptic and paraventricular nuclei manifested by hypertrophy of neurons and their nuclei occurs only with the development of hypertension and is absent in the pre-hypertensive stage.
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PMID:[Neuronal secretory activity of the hypothalamic large-cell nuclei in rats with spontaneous hypertension]. 727 96

1. The cytotoxic activity of splenic natural killer cells measured by a standard chromium release assay in urethane and alpha-chloralose-anaesthetized rats was significantly suppressed 20 min after bilateral ablation of the medial part of the preoptic hypothalamus (MPO). The suppression was completely blocked by prior splenic denervation. The splenic natural killer cell activity of MPO sham-lesioned rats or thalamus-lesioned rats, both having an intact splenic innervation, were not different from that of a non-treated control group. 2. Electrical stimulation of the bilateral MPO (0.1 ms, 0.1-0.3 mA, 5-100 Hz) suppressed the efferent activity of the splenic nerve in all six rats examined. The reduction of the nerve activity was accompanied by a transient fall in blood pressure. An I.V. injection of phenylephrine (3 micrograms/0.3 ml) also evoked a suppression of the nerve activity, which was accompanied by transient hypertension, suggesting that the suppressive effect of the MPO stimulation was independent of changes in blood pressure. On the other hand, a bilateral lesion of the MPO resulted in a sustained increase in the electrical activity of the splenic sympathetic nerve filaments which lasted for more than 2 h. 3. Microinjection of monosodium-L-glutamate (0.1 and 0.01 M in 0.1 microliters saline) unilaterally into the MPO evoked a transient suppression of the efferent discharge rate of the splenic nerve activity within 1 min, which was also accompanied by a decrease in blood pressure. The injection of saline (0.1 microliter) into the MPO had no effect. The microinjection of recombinant human interferon-alpha (200 and 2000 U in 0.1 microliter saline) into the MPO dose dependently increased the splenic nerve activity without any change in blood pressure. 4. In contrast, microinjection of interferon-alpha into the paraventricular nucleus of the hypothalamus (PVN) had no effect on splenic nerve activity, although an injection of glutamate increased the nerve activity. 5. The present results, taken together with previous reports, suggest that the neuronal networks between the MPO and the splenic sympathetic nerve, which may be activated by centrally administered interferon-alpha, are important in the suppression of the splenic cellular immunity.
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PMID:Hypothalamic modulation of splenic natural killer cell activity in rats. 812 Aug 4

Ingestion of sugars (sucrose, fructose, glucose) by various rat strains is associated with perturbations in the glucose/insulin system and higher systolic blood pressure (SBP). The association suggests causality, because alterations in insulin metabolism have been found in essential hypertension and many experimental forms of hypertension. To test the hypothesis that sugar-induced SBP elevation is secondary to perturbed insulin metabolism, we examined in 2 experiments effects of chromium and guar, substances known to affect insulin metabolism, on SBP of Spontaneously Hypertensive Rats (SHR). In both studies, sucrose compared to starch ingestion caused significant elevation of SBP; but addition of 2 chromium nicotinate complexes and guar prevented development of sugar-induced SBP elevations. The basal, genetic hypertension of the SHR was not affected by either nutrient. An additional finding in the first study was that sugar-consuming SHR supplemented with chromium had greater BW and increased organ weight (kidney, spleen, and liver) than nonsupplemented SHR. Accordingly, we have shown that two different mechanisms known to ameliorate insulin perturbations, use of chromium and guar, prevent sugar-induced SBP elevations. Since essential hypertension may be due to insulin perturbations and high dose chromium supplementation seems nontoxic, this may prove to be a useful means to lower blood pressure (BP) in some essential hypertensives, as well as diabetic hypertensives. Soluble fiber in the form of guar is also quite effective in favorably influencing sugar-induced SBP elevations.
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PMID:Effects of chromium and guar on sugar-induced hypertension in rats. 855 33

The modern diet is greatly different from that of our paleolithic forebears' in a number of respects. There is reason to believe that many of these dietary shifts can up-regulate intracellular signalling pathways mediated by free intracellular calcium and protein kinase C, particularly in vascular smooth muscle cells; this disorder of intracellular regulation is given the name 'PKC syndrome'. PKC syndrome may entail either a constitutive activation of these pathways, or a sensitization to activation by various agonists. The modern dietary perturbations which tend to induce PKC syndrome may include increased dietary fat and sodium, and decreased intakes of omega-3 fats, potassium, calcium, magnesium and chromium. Insulin resistance may be both a cause and effect of PKC syndrome, and weight reduction and aerobic training should act to combat this disorder. PKC syndrome sensitizes vascular smooth muscle cells to both vasoconstrictors and growth factors, and thus promotes both hypertension and atherogenesis. In platelets, it induces hyperaggregability, while in the microvasculature it may be a mediator of diabetic microangiopathy. In vascular endothelium, intimal macrophages, and hepatocytes, increased protein kinase C activity can be expected to increase cardiovascular risk. Up-regulation of protein kinase C in stem cells may also play a role in the promotion of 'Western' fat-related cancers. Practical guidelines for combatting PKC syndrome are suggested.
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PMID:Up-regulation of intracellular signalling pathways may play a central pathogenic role in hypertension, atherogenesis, insulin resistance, and cancer promotion--the 'PKC syndrome'. 867 54

The relation between trace elements and human health has been scarcely studied. With respect to cardiovascular diseases and hypertension attention has mostly focused on arsenic, cobalt, copper, chromium, fluorine, manganese, vanadium, zinc, selenium, silicon, cadmium, and lead. Environmental contamination can influence organ concentrations through long-term, low-level effects. This article reviews the present knowledge obtained by epidemiological, biochemical and cell biological studies. Attention is paid to interpretation problems due to the complexity of biochemical interactions with proteins of various sorts which determine metabolic processes and to the occurrence of detoxification mechanisms in which trace elements interact. This can also lead to strong variations in individual vulnerability. In general, the elements selenium, copper, zinc, chromium, and manganese seem to counteract the development of cardiovascular diseases, whereas cadmium and may be lead seem to stimulate it. Effects of arsenic, silicon and fluorine are unclear and for cobalt absent. The intensity of these effects on public health is difficult to measure, but is as yet probably limited except in extra-ordinary situations.
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PMID:Trace elements and cardiovascular diseases. 878 27

In a previous study, we found that oral chromium nicotinate overcame sucrose-induced hypertension in spontaneously hypertensive rats (SHR). Accordingly, we examined more chromium compounds to determine if others were more or less effective in regulating blood pressure (BP) of SHR. Since chromium is postulated to be an antioxidant, we also assessed the ability of different chromium compounds to alter free radical formation measured by determining thiobarbituric acid reactive substances (TBARS). The control group of SHR ingested a diet low in chromium, and 5 other groups ate the same diet with various chromium compounds added at 5 ppm-chloride, acetate, nicotinic acid-glycine-cysteine-glutamic acid (NA-AA), picolinate, and nicotinate. Following this, the rats were challenged with drinking water containing 5% and 10% w/v sucrose. Except for NA-AA, all chromium compounds inhibited the sucrose-induced elevation of systolic BP; and acetate, picolinate, and nicotinate chromium compounds lowered HbAIC below control. Only chromium acetate and nicotinate significantly lowered both hepatic and renal TBARS. Chromium picolinate lowered hepatic TBARS, and chromium chloride and NA-AA lowered neither. We conclude that chromium, rather than a specific ligand, plays a major role in ameliorating sucrose-induced BP elevations and can act as an antioxidant.
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PMID:Effects of different chromium compounds on blood pressure and lipid peroxidation in spontaneously hypertensive rats. 918 Dec 80

To assess whether acute nitric oxide (NO) blockade could unmask the vascular actions of endogenous endothelin, we tested the effects of the endothelin type A/type B (ET(A)/ET(B)) receptor antagonist bosentan and the selective ET(A) antagonist FR 139317 on blood pressure, plasma volume, and albumin escape after inhibition of NO synthesis with N(G)-nitro-L-arginine methyl ester (L-NAME). Conscious, chronically catheterized rats received L-NAME in the absence and presence of 17.4 micromol/kg (10 mg/kg) bosentan or 3.8 micromol/kg (2.5 mg/kg I.V., 10 minutes before L-NAME) FR 139317. Red blood cell volume and plasma volume were determined with chromium-51-tagged erythrocytes and iodine-125-labeled albumin, respectively. L-NAME (0.46 to 7.42 micromol/kg [0.125 to 2 mg/kg]) induced a dose-dependent increase in blood pressure, which was attenuated by 60% and 48% with bosentan and FR 139317, respectively (P<.01). L-NAME (7.42 micromol/kg) also increased hematocrit. This effect was associated with an increase in total-body albumin escape, which is reflected by a 14% reduction in plasma volume. Red blood cell volume remained unchanged. L-NAME promoted albumin escape primarily in the lung, heart, liver, kidney, and gastrointestinal tract. Both bosentan and FR 139317 markedly reduced these effects of L-NAME. Furthermore, L-NAME increased plasma levels of immunoreactive endothelin-1 from 8.6+/-0.4 (n=10) to 14.7+/-1.4 pg/mL (n=9, P<.01). These results demonstrate that the pressor response, losses in plasma volume, and increase in albumin escape observed after inhibition of NO synthesis are in part the consequence of unmasking the actions of endogenous endothelin, which are mediated predominantly via ET(A) receptors. These findings suggest a role for endogenous endothelin in the regulation of vascular functions in conditions when NO formation by endothelial cells is impaired.
Hypertension 1997 Jul
PMID:Endogenous endothelin modulates blood pressure, plasma volume, and albumin escape after systemic nitric oxide blockade. 923 16


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