Search PubMed⌕ Search

Biomedical subjects

A Amery

Publications and source records attributed to A Amery.

At least 163 records · Page 9Linked to original sources

The influence of menopause on blood pressure.

The association between menopause and systolic and diastolic blood pressure was explored in a random sample of 278 pre- and 184 post-menopausal women. In 64 subjects menopause had been surgically induced. Post-menopausal women had a higher systolic, diastolic and pulse pressure than pre-menopausal subjects (P less than 0.001). Hypertension, defined as being on antihypertensive medication, regardless of BP, or as having a pressure greater than or equal to 140/90 mmHg, was more frequently observed following menopause (40 vs 10%; P less than 0.001). After stratification by age and body mass index, the odds of having hypertension for pre- as compared with post-menopausal women were 2.2 (95% confidence interval from 1.1 to 4.4; P = 0.03). After adjustment of BP for significant covariates, such as body mass index, pulse rate and contraceptive pill intake, the slope of SBP on age was 0.5 mmHg/year (P less than 0.05) steeper in women with natural and surgical menopause than in pre-menopausal subjects. The relation of DBP with age showed a similar slope among pre- and post-menopausal subjects, but in women with natural and surgical menopause taken together, the regression line was shifted upward by an average of 2.3 mmHg (P = 0.03). The relationships of DBP with body mass index and with the urinary sodium: potassium ratio were also 0.2 mmHg/kg/m2 and 0.8 mmHg/unit steeper (P less than 0.05) in post- than in pre-menopausal subjects. In conclusion, in the present cross-sectional study menopause was accompanied by a steeper rise of SBP with age, and by an increase in the absolute level of DBP, which was independent of age.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

[The influence of menopause on blood pressure].

The association between menopause and systolic and diastolic blood pressure was explored in a random sample of 278 pre- and 184 post-menopausal women. In 64 subjects menopause had been surgically induced. Post-menopausal women had a higher systolic, diastolic and pulse pressure than pre-menopausal subjects (p greater than 0.001). Hypertension, defined as being on antihypertensive medication, regardless of blood pressure, or as having a pressure greater than or equal to 140/90 mmHg, was more frequently observed following menopause (40 vs 10%; p greater than 0.001). After stratification by age and body mass index, the odds of having hypertension for pre- as compared with post-menopausal women were 2.2 (95% confidence interval from 1.1 to 4.4; p = 0.03). After adjustment of blood pressure for significant covariates, such as body mass index, pulse rate and contraceptive pill intake, the slope of systolic pressure on age was 0.5 mmHg/year (p less than 0.05) steeper in women with natural and surgical menopause than in pre-menopausal subjects. The relation of diastolic blood pressure with age showed a similar slope among pre- and post-menopausal subjects, but in women with natural and surgical menopause taken together, the regression line was shifted upward by an average of 2.3 mmHg (p = 0.03). The relationships of diastolic blood pressure with body mass index and with the urinary sodium: potassium ratio were also 0.2 mmHg/kg/m2 and 0.8 mmHg/unit steeper (p less than 0.05) in post- than in pre-menopausal subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

[Sympathetic modification of the relationship between salt intake and blood pressure in the general population].

Using pulse rate and urinary sodium as indices of sympathetic tone and salt intake, respectively, we investigated whether both an increased sympathetic activity and a high salt consumption are needed to increase blood pressure in the population at large. A random population sample of 2081 subjects with a minimum age of 18 years was stratified by tertiles of pulse rate. In subjects with a slow and in those with a fast pulse rate, a significant curvilinear relation between blood pressure and urinary sodium was found, while in the middle pulse rate third the correlation was not significant. A significant interaction between pulse rate and urinary sodium indicated that, when urinary sodium increased from 160 to 300 mmol/24 h, both systolic and diastolic pressure rose in subjects with a fast pulse rate, but declined in those with a slow pulse rate. In conclusion, our results suggest that a high salt intake is associated with an elevated blood pressure in subjects with a high sympathetic tone, but with a decreased pressure in individuals with a low sympathetic activity.

Blood Pressure↗

Possible biochemical mechanisms involved in the antihypertensive drug-induced changes in serum lipoproteins.

The antihypertensive drug-induced changes in serum lipoproteins can be attributed to two major mechanisms, namely an increased hepatic lipoprotein synthesis and a disturbed lipoprotein catabolism. Thiazides, by inhibiting phosphodiesterase, increase the intracellular concentration of cyclic AMP leading to a stimulation of lipolysis. beta-Blockers may reduce the adenylate cyclase activity in liver cells, leading to a reduced inhibition of the liver triglyceride synthesis and a higher secretion of VLDL triglyceride particles. alpha-Blockade through phosphodiesterase inhibition and an increased cAMP level, can result in a blockade of the liver triglyceride synthesis and a reduced serum triglyceride concentration. Lipoprotein lipase activity is reduced by beta-blockers and stimulated by alpha-blockers, leading, respectively, to a lower and a higher plasma HDL cholesterol. Besides these two major mechanisms, a direct effect of antihypertensive drugs on intracellular cholesterol synthesis can also be postulated.

Animals↗

The pulmonary circulation in essential systemic hypertension.

Seventy-one men, ages 16 to 59 years, were referred for systemic hypertension, which was without detectable cause and with limited organ damage (World Health Organization stages I to II). They performed a graded exercise test on the bicycle ergometer in the sitting position. Mean brachial intraarterial pressure, mean pulmonary artery and wedge pressures and cardiac output (Fick method) were measured. At rest mean brachial artery pressure ranged from 72 to 168 mm Hg. Mean pulmonary wedge pressure was significantly (p less than 0.05) related to mean brachial artery pressure at rest, at submaximal work (50 watts) and at the end of exercise (161 +/- 42 [standard deviation] watts). In each subject pulmonary vascular resistance was calculated as the slope of the relation between the pressure gradient across the pulmonary circulation and cardiac output from data at rest, at 50 watts and at the end of exercise; mean critical closing pressure was calculated as the intercept of this relation. Pulmonary vascular resistance averaged 0.63 +/- 0.37 mm Hg/liter/min and was significantly related to age (r = 0.28, p less than 0.05) but not to rest brachial artery pressure (r = 0.14) or pulmonary wedge pressure (r = 0.09, difference not significant for both). The mean critical closing pressure averaged 6.1 +/- 4.0 mm Hg and was not related to brachial artery pressure (r = -0.08) or to age (r = -0.18, difference not significant for both). It is concluded that there is neither a primary nor a secondary effect of systemic hypertension on the pulmonary vasculature in patients with World Health Organization stages I to II essential hypertension.

Adolescent↗

Erythrocyte, plasma and urinary magnesium in men before and after a marathon.

Erythrocyte, plasma and urinary magnesium (Mg2+) concentration was measured in 23 runners before and after a marathon race. Blood samples were drawn from an antecubital vein the morning before the race (baseline), at 3 p.m. (2 h before the start), upon finishing and 12 h later. Compared with the baseline values, the intra-erythrocyte and plasma Mg2+ were decreased (p less than 0.05 or less) immediately after the marathon, from 2.13 +/- 0.16 to 2.02 +/- 0.18 mmol.l-1 cells and from 0.88 +/- 0.06 to 0.81 +/- 0.07 mmol.l-1 respectively. The Mg2+ concentration returned to pre-race values 12 h after completion of the marathon. The urinary Mg2+ excretion rate decreased (p less than 0.001) from 29 +/- 13 to 5 +/- 3 mumol.min-1 during the marathon and increased (p less than 0.05) 12 h after the race to 38 +/- 18 mumol.min-1. It is concluded that the reduction in plasma Mg2+ ion concentration during the marathon cannot be attributed to erythrocyte uptake, urinary excretion or loss in sweat. It is suggested that Mg2+ may be released from erythrocytes into the extracellular fluids during sustained exercise and taken up from these fluids by the adipose cells.

Adolescent↗

Erythrocyte 2,3-diphosphoglycerate concentration before and after a marathon in men.

Erythrocyte 2,3-diphosphoglycerate (2,3-DPG) concentration was studied in 23 runners before and after a marathon race. Blood samples were drawn from an antecubital vein the morning before the race (baseline), at 3 p.m. 2 h before the start, on finishing, and 12 and 36 h later. Compared to the baseline values, erythrocyte 2,3-DPG concentration was increased (p less than 0.001) immediately after the marathon from 4.62 +/- 0.14 to 5.56 +/- 0.13 mumol.ml-1 RBC and remained elevated 12 h later (5.45 +/- 0.14 mumol.ml-1 RBC): it returned to prerace values 36 h after completion of the marathon.

2,3-Diphosphoglycerate↗

Effects of training on erythrocyte 2,3-diphosphoglycerate in normal men.

The erythrocyte 2,3-diphosphoglycerate concentration (2,3-DPG) and the activity of red cell hexokinase, pyruvate kinase, glucose-6 phosphate dehydrogenase and glutathione reductase were studied in 27 normal volunteers before and after 2 and 4 months of physical endurance training. The 4 months of training increased maximal oxygen uptake and physical working capacity (PWC130) by 16% (p less than 0.001) and 29% (p less than 0.001) respectively. Resting heart rate was decreased (p less than 0.001) by 11 beats.min-1. With 2 months of training the erythrocyte 2,3-DPG concentration increased by 9% (p less than 0.001); with 4 months training the increase was only 4% (p less than 0.05). The training-induced increase in red cell 2,3-DPG was not accompanied by enhanced activity of erythrocyte hexokinase, pyruvate kinase, glucose-6 phosphate dehydrogenase or glutathione reductase. It is concluded that the rise in red cell 2,3-DPG induced by physical endurance training is not due to activation of red cell glycolytic enzymes or the enzymes involved in the pentose-phosphate cycle.

2,3-Diphosphoglycerate↗

Effect of calcium channel blockade and beta-adrenoceptor blockade on short graded and single-level endurance exercises in normal men.

The effect of verapamil (240 mg) on exercise capacity was studied during a short graded and a single-level endurance exercise test in 12 normal volunteers; it was compared to the effects of atenolol (100 mg x day-1). Intake of verapamil, atenolol and placebo, administered according to a randomized, double-blind cross-over design, was started 3 days before the exercise tests. Compared to placebo, verapamil did not affect peak oxygen uptake in the graded test or exercise duration in the endurance test. Heart rate, systolic blood pressure, rating of perceived exertion and respiratory data at submaximal and peak exercise were unaffected in either test. On the other hand atenolol reduced maximal oxygen uptake by 5% (p less than 0.001) and endurance exercise duration by 17% (p less than 0.05). Besides marked decreases in heart rate and systolic blood pressure during the two types of exercise, atenolol also reduced oxygen uptake at submaximal exercise levels and it increased the rating of perceived exertion (p less than 0.05), the latter only during the endurance exercise test.

Adrenergic beta-Antagonists↗

Changes in plasma lipids and apoproteins associated with physical training in middle-aged sedentary men.

The effect of endurance training on plasma lipoproteins was investigated in 27 healthy sedentary men between the ages of 20 and 55 years. During the first 4 months of the study, 13 of them (group A) participated in a training program (3 hours/wk), whereas the others served as control subjects (group B). At the end of this period the control subjects also underwent a 4-month training program. In both groups the training significantly increased physical working capacity at a heart rate of 130 bpm (PWC130), whereas it decreased the resting heart rate (p less than 0.05). Concomitantly with this improvement in cardiorespiratory fitness, a significant increase in the high-density lipoprotein (HDL) cholesterol concentration was observed (p less than 0.01); this was due to an increase in both HDL2 beta and HDL2 alpha + 3 cholesterol concentrations. The plasma total and HDL-apoprotein AI and apoprotein AII concentrations were not significantly affected by the training. Significant decreases in plasma triglyceride (p less than 0.05), very-low-density lipoprotein cholesterol (p less than 0.05), and low-density lipoprotein (LDL) cholesterol (p less than 0.001) concentrations were also observed, but only in group B, which showed a much greater increase in PWC130 at the end of the training period than group A; the decrease in the LDL cholesterol concentration in this group was accompanied by a slight decrease in the LDL-apoprotein B concentration.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Effects of opioid antagonism on the haemodynamic and hormonal responses to exercise.

1. Physical effort involves, along with an increase in the plasma concentration of beta-endorphin, profound adaptations of the circulation and the endocrine system. The effects of opioid antagonism on the responses of blood pressure, heart rate and several hormones to exercise were therefore studied in 10 normal men. They exercised in the supine position up to 33% and 66% of their maximal exercise capacity and received in a randomized double-blind cross-over protocol, either saline or naloxone (10 mg intravenously, followed by a continuous infusion of 10 mg/h). 2. Intra-arterial pressure and heart rate were continuously monitored, but were not affected by naloxone. 3. At rest, opioid antagonism produced a rise in plasma renin activity and in plasma adrenocorticotropin, cortisol and aldosterone, but only the stimulation of the two adrenocortical hormones differed significantly from the control experiments; at rest naloxone also prevented the fall in plasma adrenaline, which occurred with saline infusion. Furthermore, the exercise-induced rises in plasma angiotensin II, aldosterone, cortisol, noradrenaline and adrenaline were higher on naloxone than on saline, while a similar tendency was also present for the increases with exercise in plasma renin activity and plasma adrenocorticotropin. Neither at rest nor during exercise did opioid antagonism alter plasma lactate and glucose and serum insulin and growth hormone. 4. In conclusion, (1) endogenous opioids are not involved in the responses of blood pressure and heart rate to supine exercise; (2) at rest and during exercise, the endogenous opioids inhibit the secretion of adrenocorticotropin, aldosterone, cortisol, noradrenaline and adrenaline; (3) they also inhibit the plasma renin-angiotensin II system indirectly via the catecholamines.

Adrenal Cortex Hormones↗

Indicators of cell breakdown in plasma of men during and after a marathon race.

Plasma indicators of muscle cell leakage and of hemolysis were studied in 23 runners before and after a marathon race. Blood samples were drawn from an antecubital vein the morning before the race (baseline), at 3 p.m., i.e., 2 h before the start, on arrival, 12 and 36 h, and 7 days later. Compared with the baseline values, the plasma creatinine phosphokinase MM and MB subfractions, aldolase and glutamicoxaloacetic transaminase activity were increased immediately after the race, rose further 12 h after the marathon, and remained elevated the race, rose further 12 h after the marathon, and remained elevated 36 h and 7 days later. The plasma lactate dehydrogenase activity and myoglobin concentration were increased on arrival and returned to the pre-race activity 7 days after the marathon. Compared with the pre-race values, the plasma haptoglobin concentration was decreased immediately and 12 h after the marathon. Our data show that indicators of muscle cell leakage and of hemolysis in plasma, withdrawn after a marathon race, remained elevated for up to 7 days after the race.

Adult↗

Blood pressure during long-term converting-enzyme inhibition predicts the curability of renovascular hypertension by angioplasty.

Percutaneous transluminal renal angioplasty (PTRA) was performed in 28 hypertensive patients with 50% or more unilateral renal artery stenosis. Prospectively, the study compared the extent to which systolic (SBP) and diastolic (DBP) pressure during long-term converting-enzyme inhibition (CEI) and the ipsi- to contralateral renal vein renin ratio (RVR) predicted success of PTRA, defined as SBP less than 160 mmHg and DBP less than 95 mmHg. Both SBP and DBP after PTRA were positively correlated with pressure during CEI (P less than 0.001) and negatively with RVR (P less than 0.03). In multiple regression these associations were independent and remained statistically significant. In discriminant analysis, a SBP during CEI less than 160 mmHg, a DBP during CEI less than 95 mmHg, and a RVR greater than or equal to 1.5 identified with equal accuracy the success of PTRA. Furthermore, in patients with a SBP during CEI less than 160 mmHg, the demonstration of a RVR greater than or equal to 1.5 increased (P less than 0.05) the prediction of a positive outcome from 50 to 67%. In contrast, in 92% of the patients with a SBP during CEI greater than 160 mmHg, PTRA was not successful. Thus, blood pressure measurements during long-term CEI predict the curability by PTRA of renovascular hypertension and can be employed either alone or in association with the RVR.

Angioplasty, Balloon↗

Mortality in various intervention trials in elderly hypertensive patients: a review.

Results on total and cause-specific mortality from various randomized intervention trials on antihypertensive drug treatment in elderly hypertensives are reviewed, compared and pooled. Mortality from all causes tended to decrease in all trials, but this decrease was not statistically significant in any of the trials separately, nor when all results were pooled. When the results of all the trials were combined, there was a significant overall decrease in cardiovascular mortality of 28%. This decrease in cardiovascular mortality was mainly related to a significant reduction in cerebrovascular mortality of 41%. Mortality from coronary heart disease also tended to decrease by 28%, but statistical significance was not reached.

Aged↗

Erythrocyte and leucocyte sodium and potassium transport systems during long-term diuretic administration in men.

The effect of xipamide on the intracellular concentration and transmembrane fluxes of Na+ and K+ was studied in 12 normal male subjects, using a double-blind cross-over design. After a run-in period on placebo for 1 week, the subjects were treated with either placebo (n = 6) or xipamide 20 mg once a day (n = 6) for 16 weeks and were then switched to the alternative medication for another 16 weeks. The intra-erythrocyte and intra-leucocyte Na+ concentration was increased by 11 and 7%, respectively, during xipamide administration, while the intracellular K+ concentration was decreased by 3 and 4%, respectively. No significant effect of xipamide could however be demonstrated on the ouabain-sensitive, bumetanide-sensitive or ouabain-bumetanide-resistant 86Rb uptake and on the maximal 3H-ouabain binding in erythrocytes and leucocytes. The red cell Na+-Li+ countertransport was also not changed in the xipamide-treated subjects. Our data suggest that the increased intracellular Na+ concentration and the decreased K+ concentration in red and white blood cells of xipamide-treated subjects cannot be attributed to changes in the activity of the Na+ pump, the Na+-K+ cotransport or Na+-Li+ countertransport system or to changes in the number of active Na+ pump units.

Adult↗

Maximal aerobic power in essential hypertension.

Fifty untreated male patients aged 32 +/- 10 (s.d.) years, referred for hypertension, in whom organ damage was limited to WHO stages I and II, without underlying disease, performed a graded, uninterrupted exercise on a bicycle ergometer up to exhaustion. Mean brachial intra-arterial pressure at rest ranged from 74 to 152 mmHg. Maximal voluntary oxygen uptake was independently and negatively related to resting blood pressure (P less than 0.05), age (P = 0.05), and positively to body weight (P less than 0.05). Pulmonary wedge pressure and the components of the Fick equation--heart rate, stroke volume and arteriovenous oxygen difference--were measured in order to study the mechanisms involved. Stroke volume at peak exercise was inversely (P less than 0.05), and pulmonary wedge pressure positively (P less than 0.01), related to mean brachial artery pressure at rest. Peak heart rate was not significantly related to the severity of hypertension, but was inversely related to age (P less than 0.01). Stroke volume and pulmonary wedge pressure at the end of exercise were both similar in older and younger patients. Arteriovenous oxygen difference at peak exercise was not related either to blood pressure or to age. In conclusion, both high blood pressure and age reduce maximal voluntary oxygen uptake independently of each other by separate mechanisms; the former by an impairment of cardiac function, the latter by the limitation of peak heart rate.

Adult↗