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

Leucocyte Na+/H+ antiport activity is elevated in patients with essential hypertension and Type 1 diabetes with nephropathy. To examine the effects of hyperglycemia on the Na+/H+ antiport, normal leucocytes were incubated with 25 mmol l-1 D-glucose, L-glucose or glucose-6-phosphate for two days. Leucocyte Na+/H+ antiport activity was measured by a novel double ionophore fluorimetric method for controlling intracellular pH. Only incubation with D-glucose led to an increase in Na+/H+ antiport activity of about 31%. This effect was not due to non-enzymic glycation since glucose-6-phosphate, which glycates proteins faster than D-glucose, caused no significant difference in antiport activity. Also, osmotic effects could be excluded. Staurosporine (10 nmol l-1), a specific inhibitor of protein kinase C, prevented the rise in antiport activity due to incubation with D-glucose. As hyperglycaemia is known to increase protein kinase C activity, elevation of this kinase may be one mechanism for activation of the Na+/H+ antiport in Type 1 diabetes.
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PMID:Stimulation of the human leucocyte Na+/H+ antiport by D-glucose is mediated by protein kinase C. 166 30

The micro-heterogeneity due to varied N-linked oligosaccharides of both active- and pro-types of human urinary kallikrein (HUK) in normal subjects and some patients were investigated by the methods of serial lectin affinity chromatography and crossed affino-immunoelectrophoresis. In the case of both types of normal HUK, the species carrying tri- and/or tetra-antennary oligosaccharide(s), corefucosylated bi-antennary oligosaccharide(s), and bi-antennary oligosaccharides containing outer galactose residues and an N-acetylglucosamine residue linked beta 1,4 to a beta-linked mannose residue (bisecting N-acetylglucosamine residue) amounted to approximately 36, 33 and 17% of the total of each type of HUK, respectively. On the other hand, in some diseases, i.e. essential hypertension, Bartter's syndrome and acute pancreatitis, alterations of the chromatographic and electrophoretic patters were observed and are assumed to correspond to glycosylation changes in each HUK molecule.
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PMID:Characterization of N-linked oligosaccharides of human urinary kallikrein molecules. 261 54

Naloxone, a competitive antagonist of opioid receptors, and placebo (dextrose 5% in water (D5W) were administered on separate days to healthy normotensive (NT) male volunteers and to male patients with essential hypertension (HT). A single-blind, placebo-controlled, cross-over design was employed. Increasing doses of naloxone (0.4, 1.2, 3.6, 10.8, 32.4, 97.2 mg) were given every 30 min as slow i.v. boluses. On a separate day, i.v. boluses of D5W were given according to a similar protocol. Naloxone failed to significantly modify systolic and diastolic blood pressure (BP), heart rate (HR), respiratory rate, oral temperature or plasma catecholamines. No adverse reactions or behavioral effects were seen with naloxone. Naloxone produced a dose-dependent increase in plasma cortisol, whereas plasma cortisol showed a gradual decline on the placebo day (circadian variation). HT and NT showed similar maximal increases in plasma cortisol. Hypertensives responded to lower doses of naloxone with greater increases in plasma cortisol. The results were significantly different only if corrected by using the baseline values obtained on the placebo day. The study suggests that in awake, resting men, endogenous opioids play no role in regulating BP, HR, respiration, temperature or the activity of the sympathetic nervous system. It also suggests that the sustained elevation of BP in HT is not due to endogenous opioid substances. However, endogenous opioid substances produce a tonic inhibitory effect on the release of cortisol. This tonic inhibition seems to be greater in hypertensives than in normotensives.
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PMID:Cardiovascular and endocrine effects of naloxone compared in normotensive and hypertensive patients. 375 70

Reports on spontaneously hypertensive rats suggested that naloxone blocked the antihypertensive effects of clonidine. We compared the effects of an 8-hr intravenous naloxone infusion (6 micrograms/kg/hr) or 5% dextrose in water (D5/W) begun 2 hr before single oral doses of clonidine (0.3 mg) in six men with mild to moderate essential hypertension (EHT). Supine and standing (after 5 min) blood pressure (BP) and heart rate (HR) were measured every 20 min. Initial treatment with naloxone or placebo (D5/W) infusion was randomly allocated, with the alternate treatment given 1 wk later. Naloxone did not modify either supine or standing BP or HR. Clonidine induced a gradual, sustained reduction in both supine and standing systolic and diastolic BP and in supine HR, and there was an increase in standing HR. Naloxone did not modify the onset, maximal effect, or recovery of the hypotensive and HR effects of clonidine in both the supine and standing positions. Our data indicate that hypotensive and bradycardiac effects of clonidine in EHT are not mediated by naloxone-sensitive opioid receptors. They also suggest that opioid receptors play no role in the maintenance of hypertension nor in the BP and HR adjustments induced by postural changes in EHT.
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PMID:Naloxone does not antagonize the antihypertensive effect of clonidine in essential hypertension. 630 46

In this study we used endothelin as a paradigm to explore the concept that some vasoactive agents, acting through mobilization of Ca2+ and stimulation of protein kinase C, can interact with human skeletal muscle and modify its glucose transport. Cultured human skeletal myoblasts from the vastus lateralis demonstrated two subclasses of high-affinity endothelin receptors and a robust increase in cytosolic free Ca2+ upon exposure to endothelin. The endothelin-evoked rise in cytosolic free Ca2+ primarily resulted from Ca2+ mobilization from intracellular organelles. Both endothelin and insulin enhanced [3H]deoxy-D-glucose uptake in human myoblasts, but their effects were not additive. These findings also were observed in differentiated myotubes of L6 skeletal muscle cells. Moreover, [3H]deoxy-D-glucose uptake in human myoblasts was enhanced by treatment with phorbol 12-myristate 13-acetate. The endothelin- and insulin-mediated increases in [3H]deoxy-D-glucose were totally ablated by treatment with calphostin C. Such observations suggest that endothelin can enhance glucose uptake in human skeletal muscle. This is mediated through mechanisms that are at least partially protein kinase C dependent. Thus, increased levels of endothelin in vascular beds may contribute to altered glucose metabolism in essential hypertension.
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PMID:Endothelin mobilizes calcium and enhances glucose uptake in cultured human skeletal myoblasts and L6 myotubes. 751 52

In this study we compared the pressor, renal and endocrine effects of the physiological precursor of endothelial derived nitric oxide, L-arginine, with D-glucose, a substrate inactive on nitric oxide. Ten subjects with mild to moderate primary hypertension underwent infusion with either L-arginine (5 patients) or D-glucose (5 patients). The substances were infused over 25 min at equiosmolar rates, preceded and followed by a 25-min saline infusion. Blood pressure (BP) and heart rate were monitored at 3-min intervals; hormonal and humoral variables, inulin and para-aminohippurate clearance, and electrolyte excretion were measured at the end of each period at maximum diuresis. L-arginine and D-glucose brought about comparable increases in serum osmolality and similar hemodilution as compared with control saline. During L-arginine infusion, systolic and diastolic BP dropped by 16.6% and 11% respectively and recovered during the post-infusion period. Heart rate, plasma renin activity, and plasma norepinephrine did not change significantly. The percent BP decrease induced by L-arginine was significantly greater than that caused by D-glucose. Glomerular filtration rate remained stable, and renal plasma flow increased with both substances. However, only L-arginine stimulated markedly natriuresis, kaliuresis, and chloruresis. It also seemed to induce systemic acidosis, possibly as a consequence of hydrochloric acid generated during its metabolism. Circulating insulin, atrial natriuretic peptide, growth hormone, and glucagon levels increased, and plasma aldosterone remained unchanged during L-arginine infusion. During D-glucose infusion, insulin was stimulated and the other hormones were inhibited.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Pressor, renal and endocrine effects of systemic infusion of L-arginine in hypertensive patients]. 761 49

Essential hypertension is characterized by skeletal muscle insulin resistance but it is unknown whether insulin resistance also affects heart glucose uptake. We quantitated whole body (euglycemic insulin clamp) and heart and skeletal muscle (positron emission tomography and 18F-fluoro-2-deoxy-D-glucose) glucose uptake rates in 10 mild essential hypertensive (age 33 +/- 1 yr, body mass index 23.7 +/- 0.8 kg/m2, blood pressure 146 +/- 3/97 +/- 3 mmHg, VO2max 37 +/- 3 ml/kg per min) and 14 normal subjects (29 +/- 2 yr, 22.5 +/- 0.5 kg/m2, 118 +/- 4/69 +/- 3 mmHg, 43 +/- 2 ml/kg per min). Left ventricular mass was similar in the hypertensive (155 +/- 15 g) and the normotensive (164 +/- 13 g) subjects. In the hypertensives, both whole body (28 +/- 3 vs 44 +/- 3 mumol/kg per min, P < 0.01) and femoral (64 +/- 11 vs 94 +/- 8 mumol/kg muscle per min, P < 0.05) glucose uptake rates were decreased compared to the controls. In contrast, heart glucose uptake was 33% increased in the hypertensives (939 +/- 51 vs 707 +/- 46 mumol/kg muscle per min, P < 0.005), and correlated with systolic blood pressure (r = 0.66, P < 0.001) and the minute work index (r = 0.48, P < 0.05). We conclude that insulin-stimulated glucose uptake is decreased in skeletal muscle but increased in proportion to cardiac work in essential hypertension. The increase in heart glucose uptake in mild essential hypertensives with a normal left ventricular mass may reflect increased oxygen consumption and represent an early signal which precedes the development of left ventricular hypertrophy.
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PMID:Insulin action on heart and skeletal muscle glucose uptake in essential hypertension. 763 36

BACKGROUND AND METHODS. To determine the effects of hypertension on brain function, positron emission tomography (PET) studies using (18F)-2-fluoro-2-deoxy-D-glucose (FDG) were performed on a group of 17 otherwise healthy older hypertensive men (mean age +/- SD = 69 +/- 8 yr) and 25 age- and gender-matched controls. Subjects had medically treated essential hypertension for a minimum of 10 years (range = 10 to 24 yr) with no evidence of end-organ impairment from hypertension by routine clinical screening and by history. All hypertensive and control subjects were determined to be cognitively normal by extensive neuropsychological testing. The hypertensive subjects previously had been reported to have lateral ventricle enlargement and left hemisphere brain atrophy by quantitative MRI. PET data were analyzed using t-tests to look at group differences.
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PMID:Brain metabolic function in older men with chronic essential hypertension. 774

Clinical and experimental investigations indicate that one of the causes of primary hypertension may be diminished membrane sodium efflux. Magnesium is thought to be one of necessary factors that influence normal sodium membrane efflux and thereby maintains correct membrane gradient and potential. The aim of the study was to determinate the influence of intravenous 25% magnesium sulphate infusion on arterial pressure and sodium leukocyte membrane efflux in subjects suffering from primary arterial hypertension. The measurements were performed in 43 hypertensive patients. All patients have been divided into two groups: first-23 subjects with mild hypertension (5 women aged 32 to 50 years and 18 men aged 22 to 58 years), second-20 subjects with moderate hypertension (7 women aged 41 to 60 years and 13 men aged 28 to 65 years). The control group consisted of 31 healthy volunteers (9 women aged 37 to 55 years and 22 men aged 21 to 60 years). After venous catheter has been placed in cephalic vein standard supine arterial pressure measurements and venous blood were obtained in every person. Infusion of 20 ml 25% magnesium sulphate dissolved in 500 ml 5% dextrose was administered during 60 minutes. Again measurements were obtained after the infusion all. Arterial blood pressure was also measured 6 hours after infusion. In our investigation we proved that infusion of 20.3 mmol. of magnesium in patients with primary hypertensive disease enhanced total and furosemide-dependent but not oubain-dependent sodium membrane efflux. It did not also influence neither systolic nor diastolic arterial pressure. The greatest enhancement of total and furosemide-dependent sodium membrane efflux was observed in persons who had the greatest enhancement of magnesium blood concentration.
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PMID:[Influence of magnesium on rate of sodium transport through lymphocyte membranes in patients with hypertension]. 896 40

1. Metabolic disorders, such as obesity and non-insulin-dependent diabetes mellitus, and cardiovascular disorders, such as essential hypertension, congestive cardiac failure and atherosclerosis, have two features in common, namely relative resistance to insulin-mediated glucose uptake and vascular endothelial dysfunction. 2. Significant increases in limb blood flow occur in response to systemic hyperinsulinaemia, although there is marked variation in the results due to a number of confounding factors, including activation of the sympathetic nervous system. Local hyperinsulinaemia has a less marked vasodilator action despite similar plasma concentrations, but this can be augmented by co-infusing D-glucose. 3. Insulin may stimulate endothelial nitric oxide production or may act directly on vascular smooth muscle via stimulation of the Na+-H+ exchanger and Na+/K+-ATPase, leading to hyperpolarization of the cell membrane and consequent closure of voltage-gated Ca2+ channels. 4. There is evidence both for and against the existence of a functional relationship between insulin-mediated glucose uptake (insulin sensitivity) and insulin-mediated vasodilation (which can be regarded as a surrogate measure for endothelial function). 5. If substrate delivery is the rate-limiting step for insulin-mediated glucose uptake (in other words, if skeletal muscle blood flow is a determinant of glucose uptake), then endothelial dysfunction, resulting in a relative inability of mediators, including insulin, to stimulate muscle blood flow, may be the underlying mechanism accounting for the association of atherosclerosis and other cardiovascular disorders with insulin resistance. 6. Glucose uptake may determine peripheral blood flow via stimulation of ATP-dependent ion pumps with consequent vasorelaxation. 7. A 'third factor' may cause both insulin resistance and endothelial dysfunction in cardiovascular disease. Candidates include skeletal muscle fibre type and capillary density, distribution of adiposity and endogenous corticosteroid production. 8. A complex interaction between endothelial dysfunction, abnormal skeletal muscle blood flow and reduced insulin-mediated glucose uptake may be central to the link between insulin resistance, blood pressure, impaired glucose tolerance and the risk of cardiovascular disease. An understanding of the primary mechanisms resulting in these phenotypes may reveal new therapeutic targets in metabolic and cardiovascular disease.
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PMID:Insulin as a vascular hormone: implications for the pathophysiology of cardiovascular disease. 959 May 66


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