Showing papers by "Robert Fagard published in 1980"

Acute and chronic systemic and pulmonary hemodynamic effects of angiotensin converting enzyme inhibition with captopril in hypertensive patients

Abstract: The effects of the angiotensin converting enzyme inhibitor captopril were studied in 14 patients with essential or renovascular hypertension 75 minutes after ingestion of 25 mg of the drug, and after 2 months of therapy with 150 to 600 mg/day. Captopril acutely decreased mean brachial arterial pressure by 16.3 mm Hg (p The data indicate that the action of captopril is characterized by arteriolar and possibly venous dilatation. The increase in cardiac output during long-term treatment seems to be associated with a hypermetabolic state and in patients with very severe hypertension, with restoration to normal of mildly decreased left ventricular function.

Dose response in captopril therapy of hypertension.

Abstract: Dose-response curves of blood pressure and of the biochemical components of the renin-angiotensin-aldosterone system were determined during long-term treatment with captopril in 21 hypertensive patients. Captopril was given in biweekly, doubling doses starting with 25 mg 3 times a day until control of blood pressure was achieved or a total daily dosage of 600 mg was reached. Recumbent and standing systolic and diastolic blood pressure fell on 75 mg captopril daily. Increasing the captopril dose did not induce further significant hypotensive effects. The pretreatment level of plasma renin activity (PRA) was a poor predictor of the hypotensive effect of captopril. The rises in PRA and plasma angiotensin I level (PA I) and the decrease in plasma angiotensin II level (PA II) and plasma aldosterone level (PAC) provide biochemical evidence for angiotensin-converting enzyme (ACE) inhibition in vivo. These effects were present on daily doses of 75 to 150 mg captopril.

Biological significance of active and inactive renin in man.

Abstract: 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.

Does diet matter in hypertension

Abstract: When discussing dietary factors in hypertension, most interest now focuses on two aspects, namely the relationship between total calorie intake and hypertension and the association between sodium consumption and hypertension. However, a person who consumes an excess of calories, also ingests an excess of many foodstuffs. This review will concentrate on a discussion of total calorie consumption and sodium intake, and will refer briefly to other dietary measures such as increasing the potassium or fibre content of the diet.

First dose effect of the oral angiotensin converting enzyme inhibitor captopril

Abstract: 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.

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

Abstract: 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.

Angiotensin II and Not Sodium Status is the Major Determinant 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 [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 to 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 saralasin9s actions.

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

Abstract: 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.