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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The ratio between ankle (ASP) and brachial (BSP) systolic pressures was studied using Doppler ultrasound in 66 male subjects, 33 with sustained uncomplicated essential hypertension and 33 age-matched normal controls. 2. Based on covariance analysis, the ASP-BSP relationship was significantly different in the two populations, the ASP/BSP ratio (mean +/- SEM) being significantly lower in hypertensive subjects (106 +/- 1 vs 132 +/- 2; P less than 0.001). 3. While the ASP/BSP ratio was negatively correlated with age in normal subjects, no significant correlation was observed in hypertensive subjects. 4. The diameter of the terminal abdominal aorta measured by echography was significantly greater in hypertensive subjects, while full examination with Doppler ultrasound excluded any significant arterial stenosis of the lower limbs. 5. The study suggested that, in patients with sustained uncomplicated essential hypertension, the lower ASP/BSP ratio is related to changes in arterial wave transmission.
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PMID:The ratio between ankle and brachial systolic pressure in patients with sustained uncomplicated essential hypertension. 327 42

High blood pressure is prevalent in obesity and in diabetes, both conditions with insulin resistance. To test whether hypertension is associated with insulin resistance independently of obesity and glucose intolerance, we measured insulin sensitivity (using the euglycemic insulin-clamp technique), glucose turnover (using [3H]glucose isotope dilution), and whole-body glucose oxidation (using indirect calorimetry) in 13 young subjects (38 +/- 2 years [+/- SEM]) with untreated essential hypertension (165 +/- 6/112 +/- 3 mm Hg), normal body weight, and normal glucose tolerance. In the postabsorptive state, all measures of glucose metabolism were normal. During steady-state euglycemic hyperinsulinemia (about 60 microU per milliliter), hepatic glucose production and lipolysis were effectively suppressed, and glucose oxidation and potassium disposal were normally stimulated. However, total insulin-induced glucose uptake was markedly impaired (3.80 +/- 0.32 vs. 6.31 +/- 0.42 mg per minute per kilogram of body weight in 11 age- and weight-matched controls, P less than 0.001). Thus, reduced nonoxidative glucose disposal (glycogen synthesis and glycolysis) accounted for virtually all the defect in overall glucose uptake (1.19 +/- 0.24 vs. 3.34 +/- 0.44 mg per minute per kilogram, P less than 0.001). Total glucose uptake was inversely related to systolic or mean blood pressure (r = 0.76 for both, P less than 0.001). These results provide preliminary evidence that essential hypertension is an insulin-resistant state. We conclude that this insulin resistance involves glucose but not lipid or potassium metabolism, is located in peripheral tissues but not the liver, is limited to nonoxidative pathways of intracellular glucose disposal, and is directly correlated with the severity of hypertension.
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PMID:Insulin resistance in essential hypertension. 329 96

We investigated whether the anionic component of an orally administered sodium salt can influence the salt's capacity to increase blood pressure. In five men with essential hypertension in whom blood pressure was normal with restriction of dietary sodium chloride to 10 mmol per day (0.23 g of sodium per day), oral administration of sodium chloride for seven days, 240 mmol per day (5.52 g of sodium per day), induced significant increases in systolic and diastolic blood pressures, of 16 +/- 2 and 8 +/- 2 mm Hg (mean +/- SEM), respectively (P less than 0.05). An equimolar amount of sodium given as sodium citrate induced no change in blood pressure. Replacing supplemental sodium chloride with an equimolar amount of sodium as sodium citrate abolished the increase in blood pressure induced by sodium chloride. Both salts induced substantial and comparable sodium retention, weight gain, and suppression of plasma renin activity and plasma aldosterone, but supplemental sodium chloride increased plasma volume and urinary excretion of calcium, whereas sodium citrate did not. These preliminary findings demonstrate that the anionic component of an orally administered sodium salt can influence the ability of that salt to increase blood pressure, possibly by determining whether the salt induces an increase in plasma volume. Our observations in a small group of men with salt-sensitive hypertension will require confirmation in larger numbers of patients of both sexes.
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PMID:"Salt-sensitive" essential hypertension in men. Is the sodium ion alone important? 330 53

This study analyzed the variation in the parameters characterizing the quality of life and well-being of hypertensive patients treated with indapamide. Thirty patients (10 men and 20 women; mean age, 52.5 +/- 2.1 years, SEM) were selected after a three-week observation period during which patients received placebo. They all had essential hypertension, defined as a diastolic blood pressure between 95 and 120 mm Hg. After the three-week placebo treatment period, indapamide was prescribed as single-agent therapy at a dose of one tablet per day (2.5 mg) for three months. The quality of life and the feeling of well-being of the treated subjects were analyzed on the basis of two self-assessment scales completed by patients and on the responses to a clinical observation scale completed during the consultation by the doctor. The decrease in blood pressure was significant (p less than 0.01) by the first month of treatment and the blood pressure was controlled (diastolic blood pressure less than 90 mm Hg) in 79.3 percent of patients by the third month. Statistical analysis of the modifications in the different scores demonstrated a significant improvement between the start and the end of the indapamide treatment period for the three types of scales (p less than 0.01). Analysis of the results also confirmed the homogeneous and significant concordance between the improvement in the responses to the doctor and patient scales. These results on the improvement in quality of life and well-being observed with indapamide demonstrate the importance of taking these aspects into consideration in the drug treatment for permanent essential hypertension.
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PMID:Effects of indapamide on the quality of life of hypertensive patients. 334 88

After 12 weeks of regular exercise training in 34 patients with moderate essential hypertension, supine systolic blood pressure at rest decrease from 152 +/- 2 (means +/- SEM) to 149 +/- 2 mmHg (p less than 0.05), and diastolic blood pressure from 106 +/- 1 to 102 +/- 1 mmHg (p less than 0.001). At corresponding submaximal exercise levels, diastolic blood pressure also decreased significantly from 110 +/- 2 to 98 +/- 3 mmHg (p less than 0.001), but no significant reduction in systolic blood pressure was observed. Heart rate at the same submaximal work load was significantly reduced (p less than 0.01). This data shows that exercise training might have blood pressure lowering effect in patients with moderate essential hypertension, and might in some patients be an alternative to pharmacological treatment.
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PMID:Effect of exercise training in patients with essential hypertension. 347 52

Raised urinary calcium excretion has been reported in patients with essential hypertension, but it is not known whether this finding is an early expression of altered calcium metabolism or a consequence of longstanding high blood pressure (BP). BP and 24 h urinary excretion of calcium, sodium and creatinine were measured in a representative sample of healthy normotensive sixth grade school boys (n = 146: mean age 11.2 +/- 0.1 yrs, SEM). A significantly higher calcium output was found in children in the upper quarter of the BP distribution, even when differences due to body size, urinary creatinine and sodium excretion were excluded. The same result was obtained when students from the upper BP quartile were compared with age, height and weight-matched students from the rest of the study population (urinary calcium: 2.63 +/- 0.42 vs 1.54 +/- 0.23 mmol/24 h, P less than 0.02). Enhanced urinary calcium excretion is thus found in children in the upper part of the BP distribution for their age and sex and who are therefore at higher risk of hypertension in adulthood. This finding is compatible with the hypothesis of a primary abnormality of calcium metabolism in essential hypertension.
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PMID:Calcium metabolism and blood pressure in children. 350 24

An association between hyperinsulinemia and hypertension has been suggested by epidemiological surveys. To assess whether this association is independent of the presence of other hyperinsulinemic states, such as obesity and glucose intolerance, we measured the insulin response to oral glucose in a group of middle-aged moderately obese [144 +/- 4% overweight (mean +/- SEM)] patients (n = 18) with essential hypertension (174 +/- 5/104 +/- 2 mm Hg) and normal glucose tolerance. Normotensive subjects (n = 17) with normal glucose tolerance, matched for age and degree of overweight, served as the control group. The mean insulin response to glucose was twice as high in the hypertensive patients (25.8 +/- 0.2 mU/ml X 2 h) as in the normotensive subjects (11.3 +/- 0.2; P less than 0.001), yet the glucose incremental area was 3-fold higher in the former (10.9 +/- 1.0 g/dl X 2 h) than in the latter (3.5 +/- 0.7; P less than 0.001), thus indicating more severe insulin resistance. In the hypertensive group, systolic blood pressure levels were directly correlated with the 2-h plasma insulin values (r = 0.75; P less than 0.001). Furthermore, the 2-h plasma insulin value and the degree of overweight accounted for 65% of the variation in the systolic blood pressure in a multiple regression model (r = 0.81; P less than 0.001). We conclude that in obesity, the occurrence of hypertension marks the presence of additional hyperinsulinemia and insulin resistance, independent of any impairment of glucose tolerance.
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PMID:Evidence for an association of high blood pressure and hyperinsulinemia in obese man. 351 32

The effect of metoclopramide (10 mg, iv.) or physiological saline on the exercise-induced (standardized bicycle ergometry) increase in blood pressure and heart rate of patients with essential hypertension was investigated in a double blind, randomized, self controlled study. Metoclopramide had no effect on the exercise-induced increase in blood pressure but significantly enhanced the tachycardia due to ergometry after 4-6 min exercise. The mean slope of linear regression lines calculated from the systolic blood pressure and the corresponding heart rate measured before and during (at 1,2,3,4,5 min) exercise after metoclopramide was significantly steeper than after physiological saline (1.1 +/- 0.12 vs 0.79 +/- 0.09; mean +/- SEM), indicating the decrease in baroreflex sensitivity after metoclopramide. On the basis of results the possible role of endogenous dopaminergic mechanisms in suppressing some components of pressor effect of physical exercise can be hypothesized.
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PMID:Metoclopramide decreases baroreflex sensitivity in patients with essential hypertension. 356 Nov 60

The concentrations of unconjugated plasma dopamine (PDA) were studied in patients with various types of hypertension. Catecholamines were extracted from plasma specimens (1.0-3.0 ml) through an Amberlite CG50 (Li+-form) microcolumn and eluted by a magnesium sulfate - ethanol solution. The elute was then desalinated and deproteinized by the ethanol-treated precipitation procedure and dried in a vacuum oven at 25 degrees C. A fraction of catecholamines was assayed with the modified procedures of the COMT-mediated radio-enzymatic method. This assay system was sensitive enough to permit an accurate measurement of PDA as low as 6.0 pg per ml of plasma without any detectable contamination of the conjugated dopamine. The resting levels of PDA were 10.1 +/- 1.0 pg/ml (mean +/- SEM), 9.5 +/- 1.0 and 13.7 +/- 0.6 in patients with borderline hypertension (BH, n = 25), essential hypertension (EH, n = 22) and renovascular hypertension (RVH, n = 8), respectively. The values in EH patients were significantly smaller than those in age-matched normal controls (13.0 +/- 1.4, n = 14, p less than 0.05). Remarkably increased PDA values were observed in patients with pheochromocytoma (76.5 +/- 25.4, n = 9, p less than 0.01). Significantly raised PDA values were also found in patients with primary aldosteronism (PA, 27.8 +/- 9.0, n = 6, p less than 0.05), while their plasma norepinephrine levels (PNE, 169 +/- 39 pg/ml) tended to be lower than those of normal controls (206 +/- 20), showing an apparent dissociation between the values of PDA and PNE. Upright posture for 15 minutes induced a significant rise in PDA (p less than 0.05) in all subjects except PA patients. The postural changes of PDA, however, were invariably smaller than those of PNE (p less than 0.05). The resting values of PDA in normal, BH and EH patients showed a significant negative correlation with their mean arterial pressures (r = -0.301, n = 61, p less than 0.05) and a positive correlation with those of PNE (r = 0.381, p less than 0.01). There was no correlation between PDA and age in any group studied. These findings indicate that PDA might not be only a precursor fraction of neurotransmitters released from the sympathetic nervous system but could also represent a physiological function of the dopaminergic regulatory system. The varied but distinctive features of PDA status in various types of hypertension suggest the possibility that the peripheral dopaminergic mechanisms play an inherent role in the pathogenesis of hypertension.
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PMID:[Plasma dopamine concentrations in various types of hypertension]. 375 30

The effect of circulating arginine vasopressin (AVP) on blood pressure, heart rate and skin blood flow was investigated in 8 untreated patients with mild essential hypertension using a specific antagonist of the pressor effect of AVP. Skin blood flow was measured with a laser Doppler flowmeter and blood pressure with a Remler M2000 recorder. The study was carried out in double-blind fashion using a cross-over design. Each patient received at a 60 min interval the AVP-antagonist, d(CH2)5Tyr(Me) AVP, 5 micrograms/kg i.v., and its vehicle. The sequence of treatment phases was randomly allocated. Pretreatment plasma AVP levels averaged 1.1 +/- 0.2 pg/ml (mean +/- SEM). Neither the AVP-antagonist nor its vehicle had any effect on blood pressure, heart rate and skin blood flow as well as on plasma renin activity and plasma catecholamines. It is therefore concluded that circulating AVP does not contribute to the maintenance of blood pressure in patients with mild essential hypertension and normal plasma AVP levels.
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PMID:Blockade of the vascular effect of vasopressin in patients with mild essential hypertension. 376 22


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