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Biomedical subjects

R Fagard

Publications and source records attributed to R Fagard.

At least 397 records · Page 22Linked to original sources
PubMed1983

The effect of hemin and of allyl isopropyl acetamide on protein synthesis in rat hepatocytes.

Protein synthesis was measured in incubated hepatocytes. While hemin brings about a slight stimulation, allyl isopropyl acetamide (a compound that destroys the heme bound to cytochrome P450) inhibits protein synthesis by a mechanism that appears to result exclusively from depletion of cytoplasmic heme. Indications that in hepatocytes, as in reticulocytes, protein synthesis may be in part regulated by heme at the level of initiation are: i) that inhibition is accompanied by polysome breakdown; ii) that the protein synthesis inhibitor already isolated from rat liver, is hemin reversible iii) that hepatocyte extracts contain a Mr 38,000 phosphoprotein which comigrates with the Mr 38,000 subunit of rabbit initiation factor 2 and iv) that the phosphorylation of both of these subunits is inhibited by hemin.

Acetamides↗
PubMed1983

Long-term converting-enzyme inhibition as a guide to surgical curability of hypertension associated with renovascular disease.

Converting-enzyme inhibition as a guide to the hypotensive response to be expected from surgery was evaluated in 27 hypertensive patients with renovascular disease. Blood pressure averaged 163 +/- 5/102 +/- 2 mm Hg (mean +/- standard error of the mean) during converting-enzyme inhibition with captopril, 518 +/- 29 mg daily for 2.8 +/- 0.3 months, and stabilized at a similar level of 165 +/- 4/104 +/- 3 mm Hg during 5.0 +/- 0.6 months of postoperative follow-up, when no medication was administered. Postoperative pressure, both systolic (r = +0.53; p = 0.004) and diastolic (r = +0.55; p = 0.003), was correlated with blood pressure during converting-enzyme inhibition. In addition, multiple regression analysis identified systolic pressure during converting-enzyme inhibition as the only significant (p less than 0.01) predictor of postoperative systolic pressure. Diastolic pressure during converting-enzyme inhibition (p less than 0.05) in conjunction with circulating renin (p less than 0.05) and renin suppression from the contralateral kidney (p less than 0.01) explained up to 53% of the postoperative diastolic pressure. Therefore, blood pressure during long-term converting-enzyme inhibition may be useful as a predictor of the postoperative blood pressure in hypertensive patients with renovascular disease.

Adult↗
PubMed1983

Double-blind comparison between propranolol and bendroflumethiazide in captopril-treated resistant hypertensive patients.

In a double-blind crossover trial, 15 captopril (daily dose 600 mg) treated patients received in addition to the converting enzyme inhibitor, placebo, propranolol (240 mg), or bendroflumethiazide (7.5 mg). Propranolol produced an additional hypotensive effect, while pulse rate slowed, indicating effective beta-adrenoceptor blockade. Plasma renin activity decreased, but the hypotensive effect of propranolol was not accompanied by changes in the plasma angiotensin II and aldosterone levels or in the urinary aldosterone excretion. Also bendroflumethiazide lowered blood pressure, while body weight decreased slightly. During captopril-bendroflumethiazide treatment, serum sodium and potassium decreased while the plasma renin-angiotensin-aldosterone system was stimulated. In these captopril-treated patients, the hypotensive response to bendroflumethiazide tended to be somewhat larger than the response to propranolol, but the difference was small and statistically not significant.

Bendroflumethiazide↗
PubMed1983

Structure of the heme-regulated eukaryotic initiation factor 2 alpha kinase. End group analysis and phosphoaminoacid content.

The Mr 80,000 subunit of the inhibitor of protein synthesis that is activated in heme deficiency was purified from SDS gels. Radiolabelled reagents were used to determine the end terminal residues: the N-terminal residue was found to be only glutamine, and the C-terminal residue only valine. Phosphoaminoacids determination revealed both phosphoserine and phosphothreonine.

Amino Acids↗
PubMed1983

Electrocardiographic changes after physical training in patients with myocardial infarction.

Electrocardiographic voltage measurements were performed in 24 men with an inferior myocardial infarction before and after 14 +/- 0.5 weeks of physical training. Oxygen uptake at peak exercise increased 42% and heart rate at rest was significantly decreased after training. Increases were found in the magnitude of the R waves in leads II, aVF and V4 to V6; of the S wave in leads V1 and V3; of the T waves in V5 and V6; and of the Sokolow index of QRS voltage. Also, the magnitude of the mean electrical vector in the frontal plane was significantly higher after training. These data were compared with those derived from two electrocardiographic tracings, separated by an average of 19 +/- 1.5 weeks, of 20 other patients with an inferior myocardial infarction who were comparable in age, weight, risk factor and delay between infarction and first examination, but who were not trained. When the electrocardiographic changes between the two observations were compared for the two groups, the trained patients show significant increases in the magnitude of the R wave in the left precordial leads, and leads II and aVF and the Sokolow voltage criterion; in the magnitude of the T wave in leads V5 and V6; and in the magnitude of the mean electrical vector in the frontal plane. It is concluded that physical training in patients with myocardial infarction can alter cardiac structure, as evaluated by voltage measurements on the electrocardiogram.

Electrocardiography↗
PubMed1983

Effects of tibalosine, a new alpha-adrenoceptor antagonist, in essential hypertension.

Tibalosine is a phenylethylamine derivative known to lower arterial pressure in hypertensive animal models. In a double-blind cross-over study, 12 patients with essential hypertension, on a constant sodium intake, received placebo and tibalosine, 150 mg daily. Standing (-5.5/-6.0 mm Hg) and supine (-8.5/-7.5 mm Hg) blood pressure and standing (-7.0 bmp) and supine (-7.5 bpm) pulse rate were reduced by tibalosine. Plasma renin activity (-0.41 ng/ml/hr) and plasma angiotensin 1 (-47 pg/ml) and angiotensin II (-3.0 pg/ml) levels decreased. There were no significant changes observed in plasma aldosterone or in the urinary excretion of aldosterone, kallikrein, or prostaglandin E2, F2 alpha, and F alpha metabolites. During tibalosine treatment, creatinine clearance decreased by 20 ml/min and serum creatinine rose by 0.04 mg/100 ml. The increase in serum sodium by 0.05 mmol/l was not accompanied by significant changes in body weight. There were small, but significant reductions in hemoglobin (-0.4 gm/100 ml), hematocrit (-1.5%), and erythrocyte count (-0.15 X 10(6) cells/mm3) during tibalosine intake, while blood glucose rose by 4.0 mg/100 ml. Apart from a slight tranquilizing effect in two anxious patients, no obvious sedation was observed. Subjective complaints were as frequent during placebo as during active treatment periods.

Adrenergic alpha-Antagonists↗
PubMed1983

Four urinary cations and blood pressure. A population study in two Belgian towns.

The relationship between blood pressure and the 24-hour urinary excretion of four cations (Ca, Mg, K, Na) was investigated in a random sample of 688 inhabitants of two Belgian towns. In 160 youths aged 10-19 years, systolic/diastolic blood pressure averaged 118 +/- 12.6/65 +/- 8.6 mmHg (mean +/- standard deviation) and the urinary excretion of the four urinary cations was broadly similar in both sexes. Adjusting for body weight removed the strong relationship between blood pressure and age, but a positive relationship between systolic pressure and pulse rate emerged. The only association between blood pressure and a urinary constituent was with calcium excretion, and this correlation was no longer apparent after adjusting for weight. In 528 adults aged greater than or equal to 20 years, systolic/diastolic pressure averaged 130 +/- 14.4/77 +/- 9.8 (p less than 0.001) higher in male than in female subjects. In these adults, both systolic and diastolic pressure were strongly and independently correlated with age and body weight. Systolic pressure in women was also significantly and positively related to pulse rate (r = +0.20; p less than 0.001). After adjusting for age and body weight, systolic and diastolic pressure in men were significantly and negatively correlated (p less than 0.001 and p less than 0.01, respectively) with urinary potassium excretion. Diastolic pressure in men was weakly but positively correlated with calcium excretion (p less than 0.05 after adjusting for body weight, age and urinary potassium excretion). The present study indicates that urinary potassium is a consistent and negative predictor of both systolic and diastolic pressure in adult men, whose diastolic pressure was also weakly and positively associated with urinary calcium. In youths and female subjects, the single 24-hour urinary excretion of the four cations did not contribute to the prediction of blood pressure.

Adolescent↗
PubMed1983

Effects of prostaglandin synthesis inhibition on blood pressure and humoral factors in exercising, sodium-deplete normal man.

A double-blind placebo-controlled study was carried out in 10 sodium-deplete normal men to determine whether prostaglandin synthesis inhibition (PG-inhibition) by indomethacin (150 mg daily for three days plus an additional 50 mg on the morning of the active experiments) affected blood pressure and humoral factors at exercise. Urinary sodium excretion during placebo averaged 39 mEq/24 h. Independent of the level of physical activity, PG-inhibition increased (P less than 0.001) intraarterial systolic pressure by 12 mmHg and mean and diastolic pressure by 5 and 3 mmHg, respectively. Heart rate, body weight and exercise capacity were not significantly changed. Following PG-inhibition plasma 13,14-dihydro-15-keto-prostaglandin F alpha, plasma renin, angiotensin II and aldosterone were reduced (P less than 0.001) to a similar degree at rest and exercise. However, PG-inhibition did not abolish the exercise related stimulation of the plasma renin-angiotensin-aldosterone system. PG-inhibition had no significant effect on the plasma catecholamines nor on the urinary excretion of aldosterone and kallikrein. Twenty-four-h urinary sodium (-15 mEq; P less than 0.01) decreased. In sodium-deplete subjects prostaglandins seem to exert a depressor action on the systemic circulation, and to have a tonic influence on the renin system. Both these effects are similar at rest and exercise. Prostaglandins are probably not involved in the exercise-induced stimulation of the plasma renin-angiotensin-aldosterone system.

Adult↗
PubMed1983

Effects of beta 1-adrenoceptor agonism on plasma renin activity in normal men.

The contribution of beta 1-adrenoceptors to the regulation of plasma renin activity was investigated in nine healthy sodium-replete volunteers: seven subjects received a cumulative intravenous dose of 75 micrograms/kg prenalterol, a predominant beta 1-adrenoceptor agonist, and two subjects only vehiculum. In the seven actively treated subjects beta 1-adrenoceptor agonism increased (P less than 0.001) systolic intra-arterial pressure by an average of 16 +/- 4 mm Hg and heart rate by 19 +/- 3 beats min. These increases were significantly (P less than 0.04) different from the changes observed in the two control subjects (+ 3 +/- 4 mm Hg and -1 +/- 4 beats/min, respectively). Plasma renin activity, however, tended to decrease in both the actively (-38%) and saline (-28%) treated subjects. Predominant beta 1-adrenoceptor agonism, powerful enough to increase systolic pressure and heart rate does not increase plasma renin activity in supine sodium-replete normal man.

Adrenergic beta-Agonists↗
PubMed1983

Ventilatory thresholds during short- and long-term exercise.

The ventilatory (anaerobic) threshold for short-term exercise was defined as the work rate or O2 uptake (VO2) immediately below the work rate at which ventilation increased disproportionately relative to work rate or VO2, and the ventilatory threshold for long-term exercise as the work rate or VO2 immediately below the work rate at which ventilation continued to increase with time rather than attain a steady state. The purpose of the present study was to investigate how both thresholds relate to each other and how they relate to other measures of physical performance capacity. The subjects were eight healthy males, 20-53 yr of age. Maximal performance capacity was estimated by measurements of maximal O2 uptake (VO2 max) and by endurance performance during a 12-min distance run. A high interrelationship was found between the two thresholds (r = 0.84), and each threshold expressed in VO2 (ml X min-1 X kg-1) correlated highly with VO2 max (r = 0.87 and r = 0.75, for short-term and long-term exercise, respectively). When the two thresholds were expressed as a percentage of VO2 max, neither threshold showed a significant relationship with VO2 max. Endurance performance was significantly correlated with both the ventilatory threshold for short-term and long-term exercise (r = 0.73 and 0.82, respectively). A stepwise multiple regression analysis indicated that the distance run in 12 min was best predicted by VO2 max (R2 = 0.66) or the ventilatory threshold for long-term exercise (R2 = 0.63). It is concluded that the ventilatory threshold for long-term exercise is a more specific measure to explain running performance than is the threshold during graded exercise.

Adult↗
PubMed1983

Influence of central alpha 1 inhibition in patients with essential hypertension.

CP-804-S is a substituted phenylbutylamine, known to lower arterial pressure in hypertensive animal models. In a double-blind, crossover study, 12 patients with essential hypertension receiving a constant sodium intake received placebo and CP-804-S, 150 mg daily. Standing (-5.5/-6.0 mm Hg) and supine (-8.5/-7.5 mm Hg) blood pressures and standing (-7.0 beats/min) and supine (-7.5 beats/min) pulse rates were significantly reduced by CP-804-S. Plasma renin activity (-0.41 ng/ml/hr) and plasma angiotensin I (-47 pg/ml) and angiotensin II (-3.0 pg/ml) levels decreased significantly. No significant changes were observed in plasma aldosterone or in the urinary excretion of aldosterone, kallikrein, and prostaglandin E2, F2 alpha, and F alpha metabolite.

Adrenergic alpha-Antagonists↗
PubMed1983

Effect of bendrofluazide on the renin-angiotensin-aldosterone system and prostaglandins in captopril-resistant hypertensive patients.

In a double-blind cross-over trial 15 captopril (daily dose 600 mg) treated patients, received in addition to the converting-enzyme inhibitor, placebo or bendrofluazide (7.5 mg). Bendrofluazide lowered blood pressure, while body weight decreased slightly. During captopril-bendrofluazide treatment, the plasma renin-angiotensin-aldosterone system was stimulated, while no effect on the urinary excretion of prostaglandin E2 and F2 alpha was found.

Bendroflumethiazide↗
PubMed1983

Decrease in renal function due to sulphinpyrazone treatment early after myocardial infarction.

Twenty-nine patients with recent myocardial infarction were randomly allocated to a placebo group (n = 14) and to a group (n = 15) who received sulphinpyrazone, 4 x 200 mg daily for 7 days. Renal function significantly and transiently deteriorated in the sulphinpyrazone group compared to the placebo group. In the sulphinpyrazone group the 24 hour-urinary prostaglandin E2 and kallikrein excretion were suppressed. These data suggest that the decrease in renal function caused by sulphinpyrazone early after myocardial infarction could be mediated by an inhibition of renal prostaglandin and/or kallikrein-kinin synthesis.

Acute Kidney Injury↗
PubMed1983

The hypotensive effect of captopril in hypertensive patients is age-related.

The hypotensive action of the angiotensin-converting enzyme inhibitor captopril was investigated in 13 hypertensive patients in relation to their age, body weight, the pretreatment level of plasma renin activity (PRA), serum creatinine concentration and suppression of angiotensin II (PA II) by captopril. Captopril was administered in biweekly doubling doses (15 mg, 50 mg and finally 100 mg t.i.d.). The change in systolic blood pressure produced by captopril was significantly (p less than or equal to 0.05 or less) related to age (r = 0.67), to weight (r = 0.55), to the initial PRA levels (r = -0.63) and to the drop in PA II (r = 0.67) but not to the serum creatinine concentration. The change in diastolic blood pressure was also (p less than or equal to 0.05 or less) related to age (r = 0.59), to the pretreatment PRA level (r = -0.71) and to the fall in PA II (r = 0.70) but not to weight or to serum creatinine concentration. Our data suggest that the hypotensive action of captopril is more pronounced in younger hypertensive patients.

Adult↗
PubMed1983

The pressor effect of exogenous angiotensin II is diminished during dynamic exercise.

To evaluate the effect of dynamic exercise on the response to angiotensin II (AII), AII (7.5 ng/kg/min) or vehicle (P) was infused intravenously in seven normal sodium replete volunteers before, during and after a graded uninterrupted exercise test until exhaustion, using a randomized cross-over protocol. Plasma angiotensin II (PAII) during AII infusion was an average 86-145 pg/ml higher than during P. The differences in mean intra-arterial pressure between the AII and the P tests averaged 17 mmHg at recumbent rest, 12 mmHg in the sitting position on the bicycle ergometer and 7 mmHg at 20% of peak work rate declining progressively throughout the exercise test to become insignificant from 80% of peak work rate on. A significant difference reappeared after exercise. It is suggested that the powerful vasoconstriction in some vascular beds and the dilatation in others oppose the vasoconstricting effect of AII; other possible mechanisms are changes in pH and a decrease of the difference in log PAII between the AII and P tests with increasing levels of endogenous PAII during exercise.

Acidosis↗
PubMed1983

The effect of physical training on the left apexcardiogram.

Indices of the first derivative and of the normalized first derivative of the left apexcardiogram were used to evaluate the contractile state of the left ventricle of cyclists in the competitive season compared to their resting season and of cardiac patients before and after a physical training program. In both groups exercise capacity increased after training (P less than 0.001). The normalized first derivative of the upstroke of the systolic wave and the time from the onset of electrical depolarization to the peak value of the first derivative of the upstroke of the systolic wave were unchanged after training in both groups. Also in both groups training did not alter the height of the A-wave in percentage of the amplitude of the systolic wave nor the normalized first derivative of the A-wave. These indices suggest that the compliance of the left ventricle was not decreased despite thickened left ventricular walls as reported in both groups. Thus physical training does not seem to alter the intrinsic myocardial contractile state, as far as reflected by these indices of the left apexcardiogram.

Adolescent↗