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Biomedical subjects

F Boomsma

Publications and source records attributed to F Boomsma.

170 records · Page 10Linked to original sources
PubMed1981

Haemodynamics, plasma noradrenaline and plasma renin in hypertensive and normotensive teenagers.

1. Plasma noradrenaline, active and inactive plasma renin, cardiac index and total peripheral vascular resistance were studied in 41 subjects, initially aged 10-19 years, who were followed up for at least 2 years after a blood pressure reading of 140 and/or 90 mmHg or more (initial hypertensives) and in 41 normotensive control subjects selected from the same population and matched for age, sex and body-mass index. 2. The initial hypertensive subjects had a lower mean cardiac index (3.63 +/- SD 0.83 vs 4.00 +/- 0.89 litre min-1 m-2), a higher mean total peripheral resistance (26.8 +/- 5.7 vs 22.8 +/- 5.5 peripheral resistance (26.8 +/- 5.7 vs 22.8 +/- 5.5 units) and a higher mean plasma noradrenaline units) and a higher mean plasma noradrenaline concentration (336 +/- 146 vs 281 +/- 126 pg/ml) than the control subjects. 3. Mean plasma noradrenaline concentration was higher in initial hypertensive subjects with a high active renin concentration than in those with a normal renin concentration (442 +/- 70 vs 324 +/- 100 pg/ml). 4. A weight-adjusted standardized regression coefficient of 0.77 between active plasma renin concentration and left ventricular mass was found in normotensive control subjects. 5. These findings are at variance with the existence of a hyperkinetic phase in young hypertensive subjects and suggest that sympathetic overactivity may be related to early essential hypertension through increase of peripheral vascular resistance.

Adolescent↗
PubMed1979

Raised blood pressure and plasma noradrenaline concentrations in teenagers and young adults selected from an open population.

Plasma noradrenaline (PNA) concentrations were measured in 38 subjects aged 13-23, who were followed up for two to four years after an initial blood-pressure (BP) reading of 140/90 mm Hg or over was obtained, and in 39 age-matched controls from the same open population. Subjects who were hypertensive when the PNA concentration was measured had a significantly higher concentration (351 +/- SE 26 pg/ml) compared with their controls (248 +/- 29 pg/ml). Furthermore, in those subjects in whom the mean arterial pressure decreased by under 5% during the follow-up period the mean concentration was 363 +/- 27 pg/ml, compared with 271 +/- 29 pg/ml in their controls. PNA concentrations and systolic BP were positively correlated. A positive association between PNA concentrations and age was observed in the controls but not the subjects with hypertension, owing to the higher concentrations in younger hypertensive subjects.

Adolescent↗
PubMedDate not supplied

Psychological, cardiovascular, and endocrine changes during 6 hours of continuous infusion of epinephrine or norepinephrine in healthy volunteers.

Psychological, cardiovascular, endocrine, and metabolic reactions to a sustained infusion of epinephrine (E) and norepinephrine (NE) were studied in 10 healthy male volunteers in a placebo-controlled randomized design. The subjects participated each in three sessions during which they received 6-hr infusion of either E (82 pmol/kg/min), NE (178 pmol/kg/min), or placebo (PLA) (saline, 5.4 ml/hr). Heart rate and intra-arterial blood pressure were recorded continuously. Blood samples for assay of catecholamines, cortisol, prolactin, growth hormone, insulin, triglycerides, and glucose were obtained at regular intervals. Changes in subjective mood were assessed with the Profile of Mood States (POMS) and the State-Trait Anxiety Inventory (STAI). During infusion of E, arterial plasma epinephrine levels increased 10-fold, which induced significant increases in heart rate, plasma insulin, and glucose levels, and decreases in mean arterial pressure (MAP) and diastolic pressure (DAP). NE infusion caused a 5-fold arterial plasma norepinephrine increase and induced a significant decrease in heart rate and increases in MAP, DAP, and glucose levels. The effects were present shortly after initiation of the infusions, remained fairly constant during the 6-hr infusion period and disappeared within 1 hr after the infusions had been stopped. Changes in subjective mood were not observed during the infusions, nor after the infusions had been stopped. Infusion of E or NE also had no significant effect on systolic blood pressure, plasma prolactin, growth hormone, cortisol, and triglycerides. Our results show that moderate cardiovascular and metabolic effects can be caused by sustained increases in circulating catecholamines.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Asynchronous changes in prorenin and renin secretion after captopril in patients with renal artery stenosis.

An assay of plasma prorenin was developed in which the conversion to renin occurred under apparently optimal conditions. Some characteristics of the assay were 1) prorenin was activated by Sepharose-bound trypsin at 4 degrees C; 2) the concentration of activator was not critical provided that incubation was prolonged until renin activity had reached a plateau; and 3) this plateau was stable and had the same height as after maximal activation with acid, pepsin, plasmin or urokinase. Maximal activity with Sepharose-bound trypsin at 4 degrees C was higher than with cryoactivation, and optimal conditions were more readily reproduced than with trypsin at 37 degrees C or with acid-activation. The assay was used for measurements in peripheral and renal vein plasma after captopril in hypertensive patients with unilateral renal artery stenosis. Peripheral renin rose within 30 minutes after a first dose of captopril, 50 mg orally, and it remained high with chronic treatment. In contrast, peripheral prorenin fell initially and rose after 4 hours. These changes in peripheral plasma were related to changes in the secretion rates of the two forms of renin from the affected kidney. Thus chronic, but not acute, stimulation of renin release was associated with an increased secretion rate of prorenin. The late rise in prorenin is probably an indication of enhanced synthesis in the kidney, so that more prorenin is available for conversion. The data suggest that prorenin is indeed a biosynthetic precursor of renin and that, at least under certain circumstances, a major proportion of circulating prorenin originates from the kidney.

Captopril↗
PubMedDate not supplied

Use of natriuretic peptides for detecting cardiac dysfunction in long-term disease-free breast cancer survivors.

BACKGROUND: Plasma natriuretic peptides are increased in patients with cardiac dysfunction. N-terminal (NT-ANP) and B-type (BNP) natriuretic peptides were measured in disease-free breast cancer survivors, during long-term follow-up after epirubicin (360 mg/m2 or 450 mg/m2 cumulatively) and chest irradiation. PATIENTS AND METHODS: Plasma samples for natriuretic peptide measurement were repeated after extended follow-up in 54 patients, who had participated in 2 studies evaluating cardiotoxicity. RESULTS: From a median follow-up of 2.7 to 6.5 years, median BNP was raised almost three-fold (p<0.001). Symptomatic heart failure was now present in 2 patients. Compared to the epirubicin 360 mg/m2 group, BNP was higher (p=0.006) in the 450 mg/m2 group, with a trend (p=0.054) for higher NT-ANP. CONCLUSION: These findings suggest that anticancer therapy initiates an autonomically progressive process that may ultimately lead to symptomatic cardiac dysfunction, years after treatment. BNP measurement may be of value to identify patients requiring intensive cardiac follow-up.

Adult↗
PubMedDate not supplied

Effects of selective and nonselective beta-agonists on plasma potassium and norepinephrine.

The effects of graded infusions of the beta-agonists isoproterenol (nonselective), l-prenalterol (beta 1-selective), and salbutamol (beta 2-selective) on plasma potassium and norepinephrine were compared in subjects with borderline hypertension. Potassium levels fell with all three agonists, and norepinephrine levels rose with isoproterenol and salbutamol. These effects on potassium and norepinephrine were closely correlated and occurred at the same dose ranges as the cardiovascular responses. The fall in plasma potassium was probably caused by activation of beta-receptors, mainly on skeletal muscle, with subsequent stimulation of active sodium-potassium transport across the cellular membrane. The rise in plasma norepinephrine may have been due to activation of beta-receptors on sympathetic nerve endings. Activation of these presynaptic receptors is known to enhance the release of norepinephrine during nerve stimulation. For a given increase in heart rate and cardiac contractility, as measured by the heart rate-corrected duration of total electromechanical systole, which are mainly beta 1-responses, the effects on potassium and norepinephrine were in the order: salbutamol greater than isoproterenol greater than prenalterol. beta-Blockade with propranolol (nonselective), 80 mg four times a day, or atenolol (beta 1-selective), 100 mg once a day, antagonized the hypokalemic effect of isoproterenol as well as the rise in norepinephrine, but when isoproterenol was infused in doses high enough to overcome the blockade of the heart rate response, the effects on norepinephrine and potassium were abolished by propranolol and not by atenolol. Thus, the receptors in question appear to be of the beta 2-subtype.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Agonists↗