[Metabolic clearance of noradrenaline in humans].
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Biomedical subjects
Publications and source records attributed to A Cession-Fossion.
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The slow increase in heart rate which is observed in normal man submitted to heavy muscular exercise is due for a part to an activation of orthosympathetic cardiac activity which is blocked by beta antagonists. It is also explained by direct action of hyperthermia on the heart.
In the rat, desoxycorticosterone (3 to 10 mg p. kg) does not modify the systemic vasoconstriction provoked by noradrenaline even in presence of an excess of sodium chloride. This mineralo-steroid reduces the vasodilatation induced by isoprenaline. Sodium chloride in excess potentiates this inhibition.
In vitro, accumulation of metanephrine is described in renal cortex of the rat (tissue/medium ratio greater than 5). This accumulation is saturable and energy dependent.
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In dogs, the urinary clearance of IPNA-3H is very near GFR (ratio CIPNA-3H/GFR = 0,92). This ratio is not modified by cocaine. In our experimental conditions, we observe no tubulary secretion of IPNA-3H.
The urinary excretion of noradrenaline, adrenaline and creatinine has been studied in 22 normal young men during a sauna bath (20 minutes). The radio noradrenalinuria/creatinine is specifically increased, indicating a stimulation of the orthosympathetic system (19.6 ng.mg-1 +/- 7.9 in basal state; 30.5 +/- 15.7 in sauna bath).
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In normal subjects in basal conditions, urinary excretion of noradrenaline is directly related to the hydrostatic pressure changes induced by the body posture in the dependant parts of the venous system. Adrenaline elimination is no influenced by these factors.
In anesthetized dog, intravenous infusion of NA does not modify the relationship between [3H]-(+/-)-NA urinary clearance/GFR. Urinary excretion of NA is directly related to glomerular ultrafiltration.
In normal subjects, beta-adrenergic blockage by propranolol or pindolol reduces exercise hyperventilation (40 to 60% VO2 max).
Physical exercise in rats provokes an increase in plasma glucagon and free fatty acid concentrations. The persistence of exercise-induced glucagon stimulation in adrenodemedullated animals and conversely, its inhibition by immunosympathectomy, (-)-ropranolol, and pindolol substantiate the conclusion that stimulation of the alpha2 cells in exercise involves sympathetic stimulation of the beta-adrenergic receptors. The reduction of free fatty acid mobilization by immunosympathectomy and (-)-propranolol and its persistence after adrenodemedullation suggest that it is similarly mediated, at least in part, by adipose cell beta-sympathetic receptors.
Telmetered heart rate recordings have been ovtaine from 17 parachutists (6 during automatic jumps) 9 Catecholamine (adrenaline and noradrenaline) concentrations have been measured in urine and plasma of six of these subjects. No difference appears between heart rates recorded in the two jumps at egress and at parachute deployment. On the other hand, higher heart rate values are recorded during automatic jumps during descent and at ground impace. The urine catecholamine analysis after jump shows a statistically significant increase in adrenaline and noradrenaline concentration. It is suggested that simulation of the orthosympathetic system is due to two facts; muscular work performed during jumping and the emotional stress which it involves. The importance of these two causes varies with the jump circumstances.
Lactacidemia, catecholaminemia and blood pressure have been measured in normal rats submitted to a swimming exercise. They are overloaded (6% body weight). Lactacidemia is increased after 15 minutes swimming. Adrenalinemia and noradrenalinemia are also statisticaly increased. Blood pressure falls during the exercice period. Hypotension is prevented by beta adrenergic blockade.
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