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Biomedical subjects

J Staessen

Publications and source records attributed to J Staessen.

At least 235 records · Page 13Linked to original sources
PubMed1981

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

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 alpha 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 changes 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 alpha. There is no evidence for a role of the adrenergic systems in the hypotensive response.

Adult↗
PubMed1981

Moxaprindine in the acute treatment of ventricular arrhythmias in patients with cardiovascular disease.

The antiarrhythmic activity of intravenous moxaprindine was evaluated in 26 patients with cardiovascular disease; the mean maximum dose was 2.5 +/- 0.12 mg/kg. Ventricular extopics were completely abolished in 19 patients and significantly reduced in four patients, but were not favourably affected in three patients. In one patient with numerous runs of ventricular tachycardia, normal sinus rhythm was restored. Coupled ventricular ectopic activity always completely disappeared. At the maximum dose, the PR-interval (+27.7 +/- 3.3%), the QRS-duration (+24.6 +/- 2.2%), the QT-interval (+17.0 +/- 1.5%) and the QTc-interval (+10.8 +/- 1.2%) were significantly prolonged. The QRS morphology essentially remained unchanged. Moxaprindine caused first degree atrioventricular block in eight patients. The sinus rate was slowed at every dosage level. Nevertheless, moxaprindine could safely be administered to patients with dysfunction of the specialized conduction system, or with a damaged myocardium. Serious side effects did not occur. Moxaprindine is a promising new antiarrhythmic drug for the treatment of ventricular arrhythmias, but its value and safely in the chronic oral treatment of these arrhythmias remain to be established.

Adult↗
PubMed1981

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

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 plasma aldosterone concentration or in the urinary aldosterone excretion.

Captopril↗
PubMed1981

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

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 0.01) correlation (r = 0.74) 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 = 0.68; P less than 0.01) to the rise in plasma angiotensin II.

Adult↗
PubMed1981

Salt and blood pressure in Belgium.

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.

Adult↗
PubMed1981

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

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.

Adult↗
PubMed1980

Dose response in captopril therapy of hypertension.

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.

Adult↗
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↗
PubMedDate not supplied

A battery of DNA effect biomarkers to evaluate environmental exposure of Flemish adolescents.

The present paper deals with the evaluation of a battery of genotoxicity biomarkers in healthy Flemish adolescents and their relation with common pollutants occurring in their life environment. DNA damage as reflected by the comet assay appeared to be most sensitive to ozone (partial r(2) = 0.102, p < 0.00001), and to a lesser extent to ortho-cresol (partial r(2) = 0.055; p = 0.001) and 1-hydroxy-pyrene (1-OH-pyrene, partial r(2) = 0.031; p = 0.013). 8-hydroxy-deoxyguanosine (8-OHdG) was only related to ortho-cresol (r(2) = 0.069; p < 0.007). Interestingly, the comet assay results and urinary 8-OHdG concentrations were positively correlated with a Pearson r = 0.21 (p = 0.003, N = 200). Logistic regression models revealed significant relations between chromatid breaks and 1-OH-pyrene (relative risk (RR): 1.58; p = 0.008), and t,t-muconic acid (RR: 1.71; p = 0.014). There was no correlation between micronucleus formation or occurrence of chromosomal or chromatid breaks on the one hand and comet or 8-OHdG results on the other hand. Thus, in this study the comet assay on whole blood samples and urine 8-OHdG measurements especially appeared sensitive biomarkers for assessing the genetic effects of environmental pollutants to which adolescents may be exposed.

8-Hydroxy-2'-Deoxyguanosine↗
PubMedDate not supplied

Alpha-adrenoceptor blockade by tibalosine: hemodynamic and humoral effects at rest and during exercise, and effect of opioid receptor antagonism.

In a randomized double-blind protocol, 12 healthy male volunteers were studied twice at rest and during exercise after pretreatment for 1 week with placebo or 150 mg daily of the new alpha 1-adrenoceptor antagonist tibalosine. Six subjects received, on both experimental days, an intravenous infusion of saline and the other six received the opioid receptor antagonist naloxone. Combined measurements taken during rest and exercise showed tibalosine, on average, to decrease mean intraarterial pressure by 4.7 mm Hg and heart rate by 3.5 beats/min. Urinary volume and sodium excretion were transiently reduced by tibalosine as compared with placebo. Opioid antagonism by naloxone stimulated the pituitary-adrenal axis, but had no effect on the influence of tibalosine, as shown by hemodynamic, respiratory, and most humoral measurements. However, on interruption of exercise, opioid antagonism counteracted the inhibition of the plasma renin-angiotensin system by tibalosine, probably through the naloxone-induced increase in epinephrine release. In conclusion tibalosine reduced blood pressure at rest and during exercise independently of opioidergic mechanisms. This hypotensive action may be accompanied by sodium and fluid retention.

Adrenergic alpha-Antagonists↗