Search PubMed⌕ Search

Biomedical subjects

R Fagard

Publications and source records attributed to R Fagard.

At least 451 records · Page 25Linked to original sources
PubMed1980

Angiotensin II and not sodium status is the major determinant of the agonistic/antagonistic balance of saralasin's actions.

1. To study which factors determine the balance between the antagonistic and agonistic effects of the angiotensin II analogue [Sar1,Ala8]-angiotensin II (saralasin) in man, saralasin was infused in subjects on a 'normal' sodium intake (group 1) 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 action of saralasin was agonistic in group 3, antagonistic in group 2 and variable in group 1. 3. For groups 1 and 2 together the saralasin-induced changes of arterial pressure, of plasma aldosterone and of plasma renin were significantly related to control plasma angiotensin II but also the the 24 h urinary sodium excretion. When group 3 was included the changes remained significantly related to plasma angiotensin II but not to the urinary sodium excretion. 4. The results indicate that angiotensin II and not sodium status determines the agonistic/antagonistic balance of saralasin's actions.

Adult↗
PubMed1980

Biological significance of active and inactive renin in man.

The biological significance of active and inactive renin was investigated by comparison of an in-vitro assay of active, total and inactive plasma renin concentration (PRC), plasma renin activity (PRA) and plasma concentrations of angiotensin I and II with an in-vivo change in mean arterial blood pressure (MAP) produced by antagonism of angiotensin with treatment with saralasin and by blockade of angiotensin-converting enzyme by treatment with captopril. A significant relationship between the changes in MAP during treatment with saralasin and captopril with the pretreatment levels of PRA, active and total PRC and angiotensin II were found; while the pre-existing level of inactive renin was not a predictor for the hypotensive effect of saralasin and captopril. During treatment with saralasin and captopril significant increases in PRA, plasma angiotensin I concentration and total and active PRC were found and no change in inactive PRC was observed.

Adult↗
PubMed1980

Alpha- and beta-adrenoceptor blockade does not affect ventilation during exercise in man.

Alpha- and beta-adrenoceptor blockade does not affect ventilation during exercise in man. Med. Sci. Sports Exercise, Vol. 12, No. 5, pp. 375-379, 1980. Combined alpha- and beta-adrenoceptor blockade was used to study the role of the exercise induced stimulation of the adrenergic system on exercise hyperpnea. Twelve subjects performed an uninterrupted graded exercise test until exhaustion, before and during treatment with the alpha- and beta-adrenoceptor blocker labetalol. In the control study, plasma noradrenaline rose on the average 4.3 times during maximal exercise and plasma adrenaline 2.7 times, with similar data during labetalol. Labetalol did not affect oxygen uptake, carbon dioxide output, respiratory exchange ratio, pulmonary ventilation, nor the ventilatory equivalents for O2 and for CO2 at rest recumbent, at rest sitting, and during submaximal and maximal exercise, nor did it affect the anaerobic threshold. These findings do not substantiate a role for the adrenergic system in exercise hyperpnea in the conditions of the present study.

Adrenergic alpha-Antagonists↗
PubMed1980

Acute changes in the renin-angiotensin-aldosterone system, catecholamines and prostaglandins during captopril in man.

The acute hypotensive effect of 25 mg captopril was investigated in 26 hypertensive patients (11 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 provoked increases in plasma renin activity, active and total plasma renin concentration and angiotensin I; decreases in plasma kininase II activity, angiotensin II, aldosterone, prostaglandins E2 and F2 alpha and no changes in plasma (nor)adrenaline, dopamine and inactive renin concentration.

Adult↗
PubMed1980

First dose effect of the oral angiotensin converting enzyme inhibitor captopril.

Captopril was given orally to 24 patients with moderate to severe essential or renovascular hypertension, with variable degrees of sodium-volume depletion. Initiation of treatment resulted in orthostatic hypotension in 5 and in symptoms and signs of hypotension while still recumbent in 4; bradycardia accompanied the adverse hypotension which was relieved by iv atropine. After iv infusion of 1-2 liters of 0.9% NaCl patients cound resume their normal activities and be treated with captopril. The development of hypotension was related to the prevailing plasma renin level, which was partly determined by the degree of sodium-depletion and the aetiology of hypertension. The degree of sodium-depletion, the aetiology and severity of hypertension and heart rate did not contribute independently from plasma renin activity to the development of hypotension.

Adult↗
PubMed1979

Haemodynamic effects of captopril in hypertensive patients: comparison with saralasin.

1. Captopril (25 mg) reduced plasma angiotensin II (ANG II) by 53% (P less than 0.001) and mean brachial artery pressure (MBAP) by 18.7 mmHg (P less than 0.001) within 75 min in 26 hypertensive patients. After 2 months (on 150-600 mg/day) MBAP had decreased by 27.1 mmHg (n = 18) with no further change of plasma ANG II. delta MBAP was significantly related to control log plasm renin (PRA) and log ANG II in both conditions. 2. The acute depressor response to captopril was 11.2 mmHg greater (P less than 0.001) than delta MBAP during saralasin infusion (n = 12). 3. Heart rate slightly increased after acute administration of captopril (+3.3 beats/min; P less than 0.005), but cardiac output was not significantly affected; systemic vascular resistance decreased by 10% (P less than 0.01) with unchanged pulmonary vascular resistance. 4. During chronic administration, oxygen consumption, cardiac output and stroke volume increased by 15% (P less than 0.01), with unchanged heart rate; systemic vascular resistance had dropped by 30% (P less than 0.001). 5. Plasma ANG II and plasma aldosterone decreased, and PRA and ANG I increased acutely, with no further changes during chronic treatment.

Aldosterone↗
PubMed1978

Beta-blockers: once or three times a day?

In a double-blind, crossover trial 16 hypertensive patients were treated, in random order, with placebo, metoprolol 300 mg in a single daily dose, or metoprolol 300 mg/day in three doses. Both therapeutic regimens produced detectable plasma metoprolol concentrations and appreciable beta-blockade, estimated from exercise tachycardia, throughout the day. Fluctuations throughout the day in plasma drug concentrations and degree of beta-blockade were insignificant on the thrice-daily regimen, but they varied considerably on the single-dose regimen. Both therapeutic regimens also significantly lowered blood pressure throughout the day. Although the thrice-daily regimen again tended to produce a stronger and less fluctuating hypotensive action, the differences in hypotensive effect between the two regimens were not statistically significant. A single-dose of 300 mg of metoprolol can therefore be recommended if the only aim is to reduce blood pressure but not if a steady degree of beta-blockade is needed.

Adult↗
PubMed1978

Glucose intolerance during diuretic therapy. Results of trial by the European Working Party on Hypertension in the Elderly.

119 elderly, hypertensive patients were followed-up for 1 year and 48 for 2 years in a double-blind, randomised, controlled trial in which they received either placebo or 25-50 mg hydrochlorothiazide and 50-100 mg of triamterene daily. Half of the active treatment group also received 250 mg to 2 g methyldopa daily. After 2 years the active treatment group had an average increase in fasting blood-sugar of 9.6 mg/dl compared with an average fall of 3.1 mg in the placebo group (p less than 0.001). Blood-glucose rose by an average of 26.6 mg/dl in the active group when determined 1 hour after 50 g oral glucose and decreased by an average of 5.3 mg/dl in patients who had been on placebo for two years (p less than 0.05). The hyperglycaemic effect of diuretics appeared to be related to potassium loss since, in both groups, impairment of glucose tolerance was most marked in those in whom the serum-potassium decreased over the 2 years.

Aged↗
PubMed1978

Direct radioimmunoassay of plasma aldosterone in normal subjects.

A direct radioimmunoassay of plasma aldosterone concentration using an antibody of high specificity is described and compared to a previous chromatographic radioimmunoassay. A significant correlation was found between the plasma aldosterone concentration determined by this direct radioimmunoassay and by a radioimmunoassay including paper chromatography in 38 plasma samples obtained from patients with hypertension of various etiology. This direct radioimmunoassay of plasma aldosterone concentration is simpler and less time-consuming. A significant and similar correlation between plasma aldosterone concentration and plasma renin activity (active renin) and renin concentration (total renin) was found in normal subjects on a regular and a low sodium intake. Plasma aldosterone concentration in normal subjects was significantly and negatively related to age and to the 24-h urinary sodium excretion.

Adult↗