Search PubMed⌕ Search

Biomedical subjects

P Leonard

Publications and source records attributed to P Leonard.

88 records · Page 5Linked to original sources
PubMedDate not supplied

Assessment of neuronal uptake of noradrenaline in humans: defective uptake in some patients with essential hypertension.

1. Disappearance of tritiated noradrenaline from plasma, after infusion to steady-state, was studied to assess neuronal uptake of noradrenaline inessential hypertension. 2. Plasma tritiated noradrenaline disappearance was biexponential. Rapid removal was dependent on neuronal uptake, being slowed both in normal subjects after desipramine, and in patients with sympathetic nerve dysfunction (autonomic insufficiency). 3. In nine of thirty-eight hypertensive patients the t1/12 similarly was prolonged. Endogenous noradrenaline escaping uptake after release, and spilling over into plasma, was increased in these patients. 4. Defective neuronal uptake of noradrenaline, by exposing adrenergic recepotors to high local transmitter concentration, may be important in the pathogenesis of essential hypertension in some patients.

Adult↗
PubMedDate not supplied

Differing noradrenaline kinetics in essential hypertension and depressive illness, two diseases in which the plasma concentration of noradrenaline is sometimes elevated.

1. The rate of spill-over of noradrenaline to plasma, and neuronal noradrenaline uptake, which influences spill-over, were studied in patients with essential hypertension and depressive illness. 2. Noradrenaline spill-over was increased in seven of thirty-four patients with essential hypertension and five of eleven patients with primary depressive illness, compared with values in seventeen normal subjects (range 1.0-3.63 nmol/min per m2). 3. Faulty neuronal reuptake of noradrenaline seemed to be the cause of higher noradrenaline spill-over in patients with essential hypertension. Increased sympathetic nerve firing rates apparently were responsible in the primary depressives, despite their normal blood pressure. 4. These puzzling findings suggest that hypertension occurs when neurotransmitter excess is due to defective noradrenaline reuptake (in essential hypertension), but not chronically increased nerve firing (in depressive illness).

Adult↗
PubMedDate not supplied

Influence of variation in dietary sodium intake on biochemical indices of sympathetic activity in normal man.

The effects of variation in dietary sodium intake on biochemical indices of sympathetic activity were investigated in normal subjects. Sodium restriction for 7 days (mean urinary sodium excretion 21 mmol/day, s.e.m. = 4) increased supine plasma noradrenaline concentration significantly (1.78 nmol/l, s.e.m. = 0.23) compared to levels during medium sodium intake (1.31 nmol/l, s.e.m. = 0.14) and high sodium intake (1.35 nmol/l, s.e.m. = 0.25), when urinary sodium excretion averaged 186 (s.e.m. = 24) and 310 (s.e.m. = 43) mmol/l respectively. Plasma adrenaline concentrations did not vary significantly. During sodium restriction, the apparent release rate of noradrenaline increased significantly; noradrenaline clearance remained unchanged. No changes were observed in the heart rate response after beta-adrenoceptor stimulation with isoprenaline, suggesting that increased sympathetic activity during sodium restriction did not necessarily alter cardiac beta-receptor sensitivity. The responses to cardiac autonomic blockade with propranolol and atropine did not vary with sodium intake. These observations suggest that the sympathetic response to sodium restriction may not be generalized, excluding, in particular, the sympathetic nerves to the heart.

Adrenergic beta-Agonists↗
PubMedDate not supplied

Norepinephrine kinetics in essential hypertension. Defective neuronal uptake of norepinephrine in some patients.

To assess sympathetic nervous system function in essential hypertension, we measured the rates of release to and removal from plasma of the sympathetic neurotransmitter, norepinephrine. In normal subjects, disappearance of tritiated l-norepinephrine from plasma, after infusion to steady state, was biexponential, with t1 1/2 = 2.0 +/- 0.4 minutes (mean +/- standard deviation) and t2 1/2 = 33 +/- 15 minutes. The rapid component of removal seemed to represent neuronal uptake of norepinephrine: the t1 1/2 was lengthened by the selective inhibitor of neuronal norepinephrine uptake, desipramine; it was not changed by the extraneuronal uptake blocker, cortisol; and it was prolonged in patients with peripheral sympathetic nerve dysfunction (idiopathic autonomic insufficiency). In eight of 37 hypertensive patients, the t1 1/2 was greater than 2.8 minutes (range, 3.3-6.0 min), longer than in any normal subject; this appears to be presumptive evidence of the existence of defective neuronal norepinephrine uptake. In these patients the rate of spillover of norepinephrine to plasma, of transmitter escaping uptake after release, was 0.73 +/- 0.39 micrograms/m2/min (4.3 +/- 2.3 nmoles/m2/min), higher than in normal subjects, 0.36 +/- 0.14 micrograms/m2/min (2.1 +/- 0.8 nmoles/m2/min) (p less than 0.01). A defect in neuronal uptake of norepinephrine, by exposing adrenergic receptors to high local norepinephrine concentration, may be important in the pathogenesis of blood pressure elevation in some patients with essential hypertension.

Adolescent↗
PubMedDate not supplied

[A review about nephropathia epidemica].

We propose a review of history, aetiology, physiopathology, clinical features, treatment and prevention of nephropathia epidemica (NE) which represents the only form of Hantavirus infection in Belgium.

Hemorrhagic Fever with Renal Syndrome↗