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Biomedical subjects

J Staessen

Publications and source records attributed to J Staessen.

At least 217 records · Page 12Linked to original sources
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

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

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↗
PubMed1982

Increase in plasma aldosterone during prolonged captopril treatment.

Plasma aldosterone concentration was measured in seven patients before and during long-term angiotensin II suppression with captopril. Plasma aldosterone decreased initially from 62 to 9 pg/ml (p less than 0.01) after 1 month of captopril administration. Thereafter, it began to increase and after 1 year reached a level of 163 pg/ml, which significantly (p less than 0.01) exceeded the pretreatment value. During long-term captopril therapy, plasma renin activity remained elevated and plasma angiotensin II concentration suppressed. The mechanism responsible for the late increase in plasma aldosterone during long-term angiotensin II suppression with captopril remains to be elucidated. Body weight decreased initially, parallel to plasma aldosterone increase, but after 6 months increased again to reach its pretreatment level after 1 year. Nevertheless a sizable and lasting hypotensive effect was observed in all patients.

Adult↗
PubMed1982

The underlying heart rhythm in patients with an artificial cardiac pacemaker.

One-hundred forty-two patients with atrioventricular block (AVB) and 61 patients with sick sinus syndrome (SSS) were followed for an average of 50 months after permanent pacemaker insertion. Their underlying heart rhythms (UHR) were evaluated repeatedly by chest wall stimulation (CWS). A deficient UHR was defined as ventricular asystole lasting 4 seconds or longer. The underlying conduction disturbance increased in 14% of AVB patients, decreased in 14%, and remained constant in 68%. The occurrence of Adams-Stokes attacks before pacemaker implantation was associated with a higher incidence of deficient UHR both in AVB and SSS; a deficient UHR was seen more frequently in AVB than in SSS. Among AVB patients (1) atrial fibrillation, flutter or tachycardia and (2) sinus rhythm with incomplete AVB, especially Mobitz 1, when present before pacemaker implantation, were associated with a significantly lower incidence of deficient UHR during subsequent pacing in comparison with other AVB patients. CWS is a non-invasive method which allows the evaluation of UHR and which can contribute to the early recognition of pacemaker-dependent patients.

Aged↗
PubMed1982

Plasma prostaglandins, renin, and catecholamines at rest and during exercise in hypertensive humans.

Plasma prostaglandins (PGE and PGF alpha), catecholamine concentration, and plasma renin activity (PRA) were measured during an uninterrupted graded exercise test on the bicycle ergometer in 11 hypertensive patients. Blood was withdrawn from the brachial and pulmonary arteries after 30 min of recumbent rest, after 15 min of rest sitting, and at the final work load of the exercise test, which averaged 143 +/- 16.5 W. Exercise did not provoke a significant change in these plasma PGE or PGF alpha concentrations, whereas a rise (P less than 0.001) in arterial PRA and (nor)epinephrine concentration was observed. It is thus unlikely that PGE or PGF alpha is an important determinant of PRA release during exercise, although circulating levels of PGE and PGF alpha do not necessarily reflect release rate or activity in the kidney.

Adult↗
PubMed1982

Biological significance of active and inactive renin in hypertensive patients.

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

Adult↗
PubMed1982

Fluctuations in the plasma angiotensin I converting enzyme activity during long-term treatment with captopril.

Eight hypertensive patients on chronic captopril treatment were studied: blood pressure, plasma converting enzyme activity (pCEA) and various components of plasma renin-angiotensin-aldosterone system were measured repeatedly, immediately before and up to 7 hours after the usual morning dose of captopril in 5 patients, or a matching placebo in 3 patients. In the patients, receiving a placebo no significant changes were observed over a 7 hour period in pCEA, plasma rénin activity (PRA), plasma angiotensin II (ANG II) plasma aldosterone (PAC) and blood pressure. In patients receive captopril (200 mg) pCEA rapidly decreased, reaching after 2 hours a minimum, corresponding to nearly 20 per cent of its reference value. Thereafter pCEA increased and after 7 hours remained only slightly depressed. Within the first hour after captopril intake a small but significant decrease of ANG II and PAC was observed, while PRA and blood pressure remained unchanged throughout the study period. A continuous low pCEA level is therefore not necessary to achieve a sustained blood pressure lowering effect during chronic captopril treatment.

Adult↗
PubMed1981

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

No significant amounts of inactive renin could be demonstrated by in vivo 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.

Animals↗