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Biomedical subjects

F Boomsma

Publications and source records attributed to F Boomsma.

At least 163 records · Page 9Linked to original sources
PubMed1986

Determination of aromatic-L-amino acid decarboxylase in human plasma.

Aromatic-L-aminoacid (dopa) decarboxylase (ALAAD) was determined in human plasma by its ability to form dopamine from the substrate 3,4-dihydroxyphenylalanine in the presence of pyridoxal-5-phosphate as cofactor. Dopamine formed was quantitated by high performance liquid chromatography with electrochemical detection. A preincubation step of plasma with the cofactor and dithioerythritol was necessary to obtain optimal reaction conditions. The assay method showed good linearity and reproducibility. The inhibition pattern of the therapeutically used peripheral dopa decarboxylase inhibitors, carbidopa and benserazide, was studied and appeared to be dependent on whether the inhibitor was added before or after the preincubation step. Mean levels in 40 control subjects, in 40 patients with essential hypertension and in 15 patients with phaeochromocytoma, were 34.6 (SD 12.1), 28.5 (SD 10.9) and 34.7 (SD 18.4) mU/l respectively. In the patients with essential hypertension the enzyme level decreased with age (p less than 0.05). Very high levels were found in plasma of two patients with metastatic phaeochromocytoma and in two patients with untreated neuroblastoma, but not in two patients with neuroblastoma after chemotherapy. The method described can be used for measuring uninhibited ALAAD activity in patients treated with benserazide, as well as for measuring total, i.e. the sum of inhibited and uninhibited, ALAAD activity in patients treated with carbidopa.

Adrenal Gland Neoplasms↗
PubMed1986

Stress levels of adrenaline amplify the blood pressure response to sympathetic stimulation.

The possibility that sympathetic pressor responses are modulated by adrenaline-mediated facilitation of neuronal noradrenaline release was explored in 17 subjects with borderline hypertension. Infusion of adrenaline, which raised plasma adrenaline by a factor of 8 to 9, augmented the rise in systolic and diastolic arterial pressure induced by standardized cold pressor and isometric exercise tests. The heart rate response to these tests was not affected. When a low dose of propranolol was given on top of the adrenaline infusion before the cold pressor test, the blood pressure response to cold exposure was not different from the response observed when the test was performed during saline infusion. Plasma noradrenaline was higher during adrenaline infusion then during saline infusion, both before and after the cold pressor and isometric exercise tests, and the effect of adrenaline on plasma noradrenaline was antagonized by propranolol. These observations are consistent with the hypothesis that stress levels of circulating adrenaline may amplify sympathetic pressor responses by facilitation of the release of transmitter noradrenaline.

Adolescent↗
PubMed1985

Prevention of epinephrine-induced hypokalemia by nonselective beta blockers.

Experimental evidence is presented that activation of beta 2 adrenoreceptors causes a dose-dependent decrease in plasma potassium, probably by shifting potassium into the cell. By this mechanism epinephrine may cause hypokalemia and predispose to cardiac arrhythmias. Prevention of these effects by nonselective beta blockers may contribute to the cardioprotective action of these drugs.

Adrenergic beta-Antagonists↗
PubMed1985

Ketanserin: a possible tool for studying the role of serotonin in hypertension.

Ketanserin is a serotonin antagonist with high affinity for S2-serotonergic receptors, which mediate the vasoconstrictor effects of serotonin. It does not block the vasodilator effects of this monoamine, and it is devoid of agonist activity and serious central side effects. Ketanserin, however, also binds to alpha 1-adrenoceptors. The compound (10 mg i.v.) was given to 30 patients with essential hypertension and four normotensive patients with chronic autonomic failure, owing to an efferent sympathetic lesion. Ketanserin lowered systolic and diastolic arterial pressure by about 20%. The effects on cardiac output, cardiac filling pressures, forearm blood flow, renal blood flow, and glomerular filtration rate revealed a hemodynamic pattern compatible with dilatation of both resistance and capacitance vessels. These vasodilator effects were accompanied by moderate reflex stimulation of the heart. The drug did not alter the pressor effect of bolus injections of the alpha 1-adrenoceptor agonist phenylephrine, which contrasted with the competitive antagonism exerted by the alpha 1-adrenoceptor antagonist prazosin. Baroreflex-mediated bradycardia after phenylephrine also was not affected by ketanserin. The drug had a distinct hypotensive effect in patients with autonomic failure, despite the fact that these patients did not respond to the nonselective alpha-adrenoceptor antagonist phentolamine, 20 mg i.v. Thus, ketanserin is capable of lowering arterial pressure independently of alpha 1-adrenoceptor blockade. The results are therefore indirect evidence supporting a role of serotonin in hypertension.

Aldosterone↗
PubMed1985

Cyclic blood pressure changes in a patient with a phaeochromocytoma: role of a central oscillator?

During continuous intra-arterial pressure monitoring in an 18-year-old man with severe hypertension and a phaeochromocytoma we registered marked oscillations in blood pressure with a cycle length of 3 min (range 2-4 min) and amplitude of 40 mmHg (range 12-80 mmHg). Changes in heart rate were opposite to changes in pressure. The pressure waves almost invariably appeared at rest and were most prominent during sleep. Plasma levels of noradrenaline were between 180-240 nmol/l but failed to show cyclic fluctuations. Plasma adrenaline and dopamine were normal. The waves disappeared during blockade of ganglionic nerve transmission (trimetaphan) and finally after surgical removal of the tumour. A cerebral ischaemic pressor response related to local vasoconstriction and leading to baroreflex mediated feedback oscillation of sympathetic neuron activity might be responsible for these pressure waves. A central oscillator mechanism somehow amplified by high circulating noradrenaline is another possibility.

Adolescent↗
PubMed1985

Compound ICI 118,551, a beta 2-adrenoceptor antagonist, lowers blood pressure.

Adrenaline may increase noradrenaline release and enhance sympathetic pressor effects through activation of pre-synaptic beta 2-adrenoceptors. Conversely, blockade of beta 2-receptors could lead to a fall in blood pressure. To test this hypothesis we performed a double-blind placebo controlled crossover study in nine patients with mild hypertension, comparing the effects of the beta 2-selective blocker ICI 118,551, 50 mg t.i.d. with those of propranolol, 80 mg t.i.d. Two hours after the first dose of ICI 118,551 or propranolol, plasma noradrenaline and blood pressure remained unchanged while heart rate and renin were reduced. After 1 week, blood pressure was significantly reduced by both drugs. The beta 2-selectivity of ICI 118,551 was confirmed by isoprenaline infusion studies. After 1 week of treatment ICI 118,551 had no effect on the beta 1-receptor mediated shortening of electromechanical systole (QS2I), the rise in systolic pressure and rise in renin, whereas these responses were blocked by a dose factor of eight after propranolol. ICI 118,551 and propranolol equally blocked the beta 2-receptor mediated fall in diastolic pressure and the rise in noradrenaline. We conclude that beta 2-selective blockade by ICI 118,551 lowers blood pressure. This finding is compatible with a role of pre-synaptic beta 2-receptors in blood pressure control.

Adrenergic beta-Antagonists↗
PubMed1983

Cardioprotection by blockade of beta 2-adrenoceptors.

The effects of different beta-adrenoceptor agonists and antagonists on plasma noradrenaline and potassium concentrations were studied in patients with borderline hypertension. Heart rate, arterial pressure and the heart rate corrected duration of total electromechanical systole (QS2I) were also measured. Infusion of the beta-adrenoceptor agonists isoprenaline (non-selective) and salbutamol (beta 2-selective), but not prenalterol (beta 1-selective) caused dose-dependent increments in plasma noradrenaline. Isoprenaline and salbutamol decreased plasma potassium dose-dependently. For a given effect on heart rate and QS2I the fall in potassium was less pronounced after prenalterol. The effects of isoprenaline were also studied after the beta-adrenoceptor antagonists propranolol, 320 mg day-1 for 1 week (non-selective) and atenolol, 100 mg day-1 for 1 week (beta1-selective). The effects of isoprenaline, when infused in equipotent chronotropic doses, on noradrenaline and potassium were not affected by atenolol, whereas they were completely abolished by propranolol. The rise in noradrenaline during beta-adrenoceptor stimulation could be explained by presynaptic facilitation of noradrenaline release. The fall in potassium probably reflects stimulation of Na-K-ATPase dependent transport of potassium into the cell. Both effects were seen after beta 2- but not after beta 1-adrenoceptor stimulation. Hypokalaemia and raised levels of noradrenaline are also known to occur under such stressful conditions as acute myocardial infarction, when circulating levels of the endogenous beta 2-adrenoceptor agonist adrenaline are high. Blockade of these effects by beta-adrenoceptor antagonists may contribute to the cardioprotective effect of these drugs. This warrants further consideration of the clinical significance of beta-blocker selectivity.

Adrenergic beta-Agonists↗
PubMed1983

Effects of captopril in acute and chronic heart failure. Correlations with plasma levels of noradrenaline, renin, and aldosterone.

The angiotensin-converting enzyme inhibitor, captopril, was given to 19 patients with severe heart failure. Seven patients had acute myocardial infarction and the remainder had chronic myocardial damage caused by ischaemia or valvular disease. Cardiac filling pressures were raised in all, the pulmonary capillary "wedge" pressure being 17 mmHg or more. Captopril, 50 mg orally, raised stroke volume and cardiac output, and reduced heart rate, cardiac filling pressures, systemic arterial pressure, and the plasma concentrations of aldosterone and noradrenaline. These changes were attended by clinical improvement. Decrements in cardiac filling pressures, systemic arterial pressure, and total peripheral resistance were positively correlated with pretreatment plasma renin. Long-term treatment with captopril was offered to 14 patients. Four patients with severe coronary disease died suddenly after initial clinical improvement. In nine patients haemodynamic measurements were repeated after three months. The results showed sustained effects on cardiac output and filling pressures but there was no loss of body weight. The haemodynamic effects were at least as good as with previous vasodilators. The fall in systemic arterial pressure, however, was greater with captopril. Captopril may become a valuable adjunct to the treatment of acute and chronic heart failure, but more information about its effect on coronary blood flow is required.

Aged↗
PubMed1983

Evaluation of a test kit for the rapid and simple colorimetric measurement of angiotensin I-converting enzyme in serum.

We have evaluated a recently introduced colour test kit for the determination of serum angiotensin I-converting enzyme catalytic activity. p-Hydroxyhippuric acid, liberated from p-hydroxyhippuryl-L-histidyl-L-leucine by angiotensin I-converting enzyme, is converted into a quinoneimine dye with an absorption maximum at 505 nm. The procedure shows excellent linearity over the whole range of catalytic activities found in serum. Intra- and inter-assay coefficients of variation are 2-5 and 7-10% respectively. Correlation with a modified Cushman-Cheung ((1971) Biochem. Pharmacol. 20, 1637-1648) method currently used in our laboratory is good, with r = 0.985 and a regression equation of y (colour kit) = 0.423 x (Cushman-Cheung) + 0.765. Haemoglobin, lipids, bilirubin and prednisone do not interfere but uric acid in concentrations higher than 600 mumol/l does. No extraction step is required. The assay is very rapid, and more than twenty samples can be determined in an hour.

Analysis of Variance↗
PubMed1983

Beta-receptor stimulation by adrenaline elevates plasma noradrenaline and enhances the pressor responses to cold exposure and isometric exercise.

Isoprenaline 3.5-35 ng/kg/min, salbutamol 17.5-175 ng/kg/min and prenalterol 1-32 micrograms/kg were given intravenously (i.v.) to 10, 12 and nine subjects with borderline hypertension respectively. For a given chronotropic effect the effects on plasma noradrenaline were in the order: salbutamol greater than isoprenaline greater than prenalterol, indicating that the increase in noradrenaline was a beta 2-receptor-mediated response. This was supported by the antagonistic effects of atenolol and propranolol on this response. Adrenaline 30 ng/kg/min i.v. raised plasma adrenaline by a factor of 10 in 17 subjects with borderline hypertension. Plasma noradrenaline rose from 218 +/- 29 to 264 +/- 35 pg/ml (mean +/- s.e.m., P less than 0.05). The increments in blood pressure and plasma noradrenaline in response to cold exposure and isometric exercise were greater during the adrenaline infusion than during saline. This effect of adrenaline was antagonized by propranolol 0.5 mg i.v. These in vivo results lend support to the view that adrenaline may act as a physiological modulator of sympathetic neurotransmission by facilitating the release of noradrenaline through activation of presynaptic beta 2-type receptors.

Acclimatization↗
PubMed1982

Treatment of hypertension with ketanserin, a new selective 5-HT2 receptor antagonist.

The new selective 5-HT2 receptor blocking agent ketanserin was given in a dose of 10 mg intravenously to 12 patients with essential hypertension. It caused a distinct fall in supine systemic arterial, right atrial, pulmonary artery, and pulmonary capillary "wedge" pressures. Cardiac output, renal blood flow, and glomerular filtration rate showed no persistent changes. Thus 5-HT2 receptor blockade caused dilatation of both resistance and capacitance vessels and of the renal vascular bed. Heart rate and plasma concentrations of renin and noradrenaline rose after ketanserin. These data suggest that 5-HT may have a role in maintaining high blood pressure.

Adult↗
PubMed1982

Activation of plasma prorenin by plasminogen activators in vitro and increase in plasma renin after stimulation of fibrinolytic activity in vivo.

Plasminogen can be activated by intrinsic activators that circulate in plasma in a precursor form, by extrinsic activator originating from tissues or the vessel wall and by the exogenous activators, urokinase and streptokinase. Tissue activator and vascular activator are probably identical. Dialysis of plasma against pH 4.0 buffer causes denaturation of the plasmin inhibitors, alpha 2-antiplasmin and C1-inhibitor, while alpha 2-macroglobulin is left intact. Incubation of pH 4.0-pretreated plasma with urokinase or streptokinase at pH 7.5 led to activation of plasminogen and prorenin. Incubation of a plasma fraction, which contained plasminogen and prorenin but no alpha 2-antiplasmin and renin, with highly purified tissue plasminogen activator also led to activation of prorenin. The vasopressin analogue, 1-desamino-8-D-arginine vasopressin (DDAVP), is a potent stimulant for the release of extrinsic activator into the bloodstream. After infusion of DDAVP, 0.4 micrograms/kg, into normal subjects, parallel increments in plasma fibrinolytic activity and renin were observed. Infusion of DDAVP into patients with type IV hyperlipoproteinaemia had little effect on plasma fibrinolytic activity and the response of plasma renin was also subnormal. These observations warrant further studies on a possible role for plasminogen activators in prorenin activation in vivo.

Cold Temperature↗