Showing papers by "Robert Fagard published in 1981"

Rise in plasma concentration of aldosterone during long-term angiotensin II suppression.

Abstract: The plasma concentration of aldosterone was followed in seven hypertensive patients before and during long-term angiotensin II suppression with the orally active angiotensin-I-converting-enzyme inhibitor, captopril. The plasma concentration of aldosterone decreased initially from 74 to 21 pg/ml (P less than 0.05) after 1 month of administration of captopril. Thereafter the plasma concentration of aldosterone began to rise and after 1 year reached a level of 165 pg/ml. During long-term captopril therapy the plasma renin activity remained increased and the plasma angiotensin II concentration suppressed. The mechanism responsible for the late rise of the plasma concentration of aldosterone during long-term angiotensin II suppression with captopril remains to be elucidated. A sizeable and lasting hypotensive effect was observed in all patients.

Effect of chronic diuretic treatment on the plasma renin-angiotensin- aldosterone system in essential hypertension.

Abstract: 1 Chronic treatment with a constant dose of hydrochlorothiazide or tienilic acid increases plasma renin activity (PRA) acutely to reach a maximum within the first week 2 During chronic diuretic therapy from 1 month to 1 year, PRA remained elevated at a rather constant level, though this was somewhat lower than the maximum level reached after 1 week 3 A significant (P less than 001) correlation (r = 074) between changes in plasma angiotensin II and renin activity provoked by chronic treatment for 3 months with hydrochlorothiazide and tienilic acid was found 4 The increase in plasma aldosterone during chronic treatment with hydrochlorothiazide and tienilic acid (1000 mg) is related (r = 068; P less than 001) to the rise in plasma angiotensin II

Salt and blood pressure in Belgium.

Abstract: Blood pressure, pulse rate, body weight, and height were measured on two occasions in the inhabitants of a random 10% sample of households in a Belgian village. Twenty-four-hour urinary excretion of creatinine, sodium, and potassium was also determined. In subjects over the age of 19 there was a significant correlation for both systolic and diastolic pressure with age and body weight and, in women, also with pulse rate. After adjusting for these three variables, the systolic blood pressure in men was negatively correlated with the daily urinary potassium excretion, and the diastolic blood pressure in women negatively with the urinary sodium: creatinine ratio. The present data, obtained within one society, do not support a role for dietary sodium in the distribution of blood pressure within this population. Comparison of the present results with data from other countries does not refute the salt-genetic hypothesis but suggests also that a high potassium intake may lower blood pressure.

The hypotensive effect of propranolol in captopril-treated patients does not involve the plasma renin--angiotensin--aldosterone system.

Abstract: 1. With a double-blind cross-over protocol, 20 hypertensive captopril-treated patients were studied by adding in a variable sequence a placebo and propranolol (80 mg three times a day) to their captopril regimen (200 mg three times a day), during periods each lasting 1 month. During captopril—placebo treatment their diastolic blood pressure remained elevated between 90 and 114 mmHg. 2. The additional administration of propranolol produced a significant hypotensive effect, but no alterations of the plasma angiotensin II and aldosterone concentrations and of the urinary aldosterone excretion occurred. The present data indicate that in captopril-treated patients the hypotensive effect of propranolol is achieved independently of changes in the plasma angiotensin II and aldosterone concentration. 3. The additional administration of propranolol also produced an increase in the serum potassium levels in the absence of any change in the plasma aldosterone concentration or in the urinary aldosterone excretion.

Role of various vasodepressor systems in the acute hypotensive effect of captopril in man

Abstract: The acute hypotensive effect of captopril 25 mg was investigated in 26 hypertensive patients (11 with essential and 15 with renal arterial disease). Intra-arterial blood pressure was recorded continuously and arterial blood was sampled for renin, angiotensin I and II, aldosterone, kininase II, catecholamines and prostaglandins. Captopril led to an increase in plasma renin activity, active and total plasma renin concentration and angiotensin I, a decrease in plasma kininase II activity, angiotensin II, aldosterone, prostaglandins E2 and F2* and no change in plasma (nor)adrenaline, dopamine and inactive renin concentration. The hypotensive effect of captopril was related to the changes in plasma angiotensin II level and inversely to the change in prostaglandin E2; the correlation coefficients were low, respectively 0.61 and −0.44. It is likely that the acute hypotensive effect of captopril to some extent is related to changes in plasma angiotensin II and in prostaglandins E2 and F2*. There is no evidence for a role of the adrenergic systems in the hypotensive response.

Mechanism of Captopril-Induced Agranulocytosis

Abstract: SummaryA case of reversible agranulocytosis in a young captopril treated patient with renovascular hypertension who was otherwise in good health is reported. Captopril was the only drug administered.Coculturing the patient’s bone-marrow with captopril in concentrations up to 104 M did not influence colony nor cluster growth at 11 days of culture. This result suggests that captopril exerts its myelotoxic effect via an indirect mechanism. The associated serum-sickness-like syndrome, the transient development of antinuclear antibodies, and the finding of circulating immune complexes support the hypothesis of a captopril induced immunodysregulation, leading to agranulocytosis.

Active and inactive renin in dog plasma before and after bilateral nephrectomy.

Abstract: No significant amounts of inactive renin could be demonstrated by in vitro treatment (acidification or cryotreatment) of dog plasma obtained before and after bilateral nephrectomy. After bilateral nephrectomy, total and active renin were cleared from the plasma following similar disappearance curves, and dropped to half of their initial value within 30 min.

Role of the renin-angiotensin and of the adrenergic system in the blood pressure regulation at exercise in normotensive subjects and in hypertensive patients.

Abstract: The haemodynamic adaptations at graded exercise were studied in normal subjects and in hypertensive patients. In an attempt to investigate the specific role of the renin-angiotensin system and of the

Angiotensin II and sodium as determinants of the agonistic--antagonistic balance of saralasin's actions.

Abstract: 1. To study which factors determine the balance between the antagonistic and agonistic effects of the angiotensin II analogue [Sar 1 ,Ala 8 ]angiotensin II (saralasin) in man, saralasin was infused in subjects on a ‘normal’ sodium intake (group 1) and during sodium restriction with appropriately elevated plasma angiotensin II levels (group 2), and in sodium-restricted subjects in whom plasma angiotensin II was suppressed by converting-enzyme inhibition with captopril (group 3). 2. The saralasin-induced increase of plasma aldosterone concentration in group 1 was different ( P per se that is associated with the antagonistic action of saralasin on the adrenal receptors. 3. On average mean intra-arterial pressure at 30 min was not affected by saralasin in group 1, had decreased in group 2 and increased ( P 4. Although saralasin did not affect plasma renin activity in group 1, plasma renin rose in group 2 and was reduced by 40% ( P

Influence of beta-adrenergic blockade on the effects of physical training in patients with ischemic heart disease

Abstract: Reduction in heart rate during submaximal exercise is often used to judge the progress of patients with ischaemic heart disease in the course of a physical training programme. Some patients, however, are treated with beta adrenergic blocking drugs and it remains controversial if chronic beta blockade influences the effects of training and if heart rate remains a useful guide in the evaluation of the state of training of these patients. Male postinfarction patients, 15 treated with and 15 without beta blockers, were trained for three months, three times a week. Cardiorespiratory results from uninterrupted incremental exercise tests before and after training were compared. In each subgroup, the heart rate and systolic blood pressure were significantly reduced. For heart rate the decrease after training became more pronounced with increasing work load and the overall reduction was significantly less in the beta blocker group compared with the patients not treated with beta blockers. For systolic blood pressure the training-induced reductions were more pronounced in the patients on beta blockers. The increase of peak oxygen uptake was similar in the patients with and without beta blockers, namely 36% and 34.5%. At submaximal exercise carbon dioxide output, pulmonary minute ventilation, and the respiratory exchange ratio were lower after training, and these effects of training were similar whether or not the patients were on beta blockers. The study shows that the usual effects of training are observed in patients on beta blockers, and that heart rate remains a useful guide to their evaluation throughout a physical training programme.