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noradrenaline/hypoxie
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[Hypoxia-induced increase in nerve activity of rabbit carotid body mediated by noradrenaline].
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The responses of 39 hypoxia-sensitive units of chemoreceptive afferent in sinus nerve to noradrenaline (NA) and its antagonist were recorded in carotid body-sinus nerve preparations from 30 rabbits. The results are as follows. (1) Discharges of the units increased from 0.13 +/- 0.06 to 0.25 +/- 0.12
Noradrenaline release from the rat heart during anoxia: effects of changes in extracellular sodium concentration and inhibition of sodium uptake mechanisms.
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1. Anoxic perfusion of the isolated rat heart releases noradrenaline in the absence of sympathetic nerve fibre stimulation. 2. Anoxic noradrenaline release is enhanced by reducing the extracellular Na+ concentration, consistent with the proposal that such release occurs by carrier-mediated efflux.
Nonexocytotic noradrenaline release induced by pharmacological agents or anoxia in human cardiac tissue.
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In acute myocardial ischemia, noradrenaline is released locally from sympathetic varicosities by a Ca(2+)-independent nonexocytotic release mechanism that is effectively suppressed by inhibitors of the neuronal noradrenaline carrier (uptake1). The purpose of the present study was to elucidate the
Paradoxical action of desipramine on the modulatory effect of bradykinin on noradrenaline release in a model of metabolic anoxia in rat isolated atria.
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We have previously shown that bradykinin (BK) can modulate the release of noradrenaline (NA) in a model of metabolic anoxia in the rat isolated atria. In this study, we tested the effect of an inhibitor of NA reuptake, desipramine, on the modulatory action of BK on NA release in this experimental
Effects of hypoxia upon contractions evoked in isolated rabbit pulmonary artery by potassium and noradrenaline.
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1. Comparisons have been made between rabbit thoracic aorta and main pulmonary artery of the effects of hypoxia upon contractions evoked by noradrenaline (NA) and KCl (K+). 2. Contractions were evoked in cylindrical sections of pulmonary artery and aorta, mounted for isometric recording of tension,
[Relationship of the activity of cardiac cholinergic mechanisms to the state of the sympathetic innervation and its noradrenaline content in hypoxia].
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Preliminary sympathectomia depletes acetylcholine (ACh) in the heart of rabbits under hypoxia. In these conditions the inhibitory action of ACh on the rat isolated heart is reduced under the noradrenaline content fall, while under increase it is potentiated. Under hypoxia noradrenaline increases
Differential effects of hypoxia upon contractions evoked by potassium and noradrenaline in rabbit arteries in vitro.
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1. A study has been made on isolated sections of rabbit femoral, renal and saphenous arteries of the effects of graded hypoxia (reducing bath PO2 from 110 mmHg, normoxia, to 55, 23 and 6 mmHg) upon contractile responses evoked by noradrenaline (NA) and KCl to 80% of maximum. 2. Potassium-evoked
Metabolic requirements for release of endogenous noradrenaline during myocardial ischaemia and anoxia.
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The metabolic conditions required for noradrenaline (NA) release from ischaemic and anoxic perfused hearts of the rat were studied. Forty minutes of flow reduction to approximately 0.25 ml g-1 min-1 did not elicit enhanced noradrenaline overflow from the isolated heart perfused with normoxic
Noradrenaline enhances angiotensin II responses via p38 MAPK activation after hypoxia/re-oxygenation in renal interlobar arteries.
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OBJECTIVE
Hypoxia and sympathetic activation are main factors in the pathogenesis of acute kidney injury (AKI). We tested the hypothesis that noradrenaline (NE) in combination with hypoxia aggravates the vasoreactivity of renal arteries after hypoxia/re-oxygenation (H/R). We tested the role of
Neuropeptide Y is released together with noradrenaline from the human heart during exercise and hypoxia.
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The myocardial release of neuropeptide Y-like immunoreactivity (NPY-LI) and noradrenaline (NA) during exercise with and without arterial hypoxia was measured in 18 healthy men by arterial (a) and coronary sinus (cs) catheterization. Exercise was performed in the supine position on a cycle ergometer
Hypoxia enhances [3H]noradrenaline release evoked by nicotinic receptor activation from the human neuroblastoma SH-SY5Y.
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We have used the human sympathetic neuronal line SH-SY5Y to investigate the effects of hypoxia on noradrenaline (NA) release evoked by either raised [K+]o (100 mM) or the nicotinic acetylcholine receptor (nAChR) agonist dimethylphenylpiperazinium iodide (DMPP). NA release was monitored by loading
Effects of chronic systemic hypoxia on contraction evoked by noradrenaline in the rat iliac artery.
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Comparisons were made between responses evoked by noradrenaline (NA) in iliac artery rings from normoxic (N) rats and chronically hypoxic (CH) rats kept in 12 % O(2) for 3-4 weeks. At P(O(2)) of 100 mmHg, cumulative concentration-response curves (CCRC) to NA were greatly depressed in
Modulation of noradrenaline release by B1 and B2 kinin receptors during metabolic anoxia in the rat isolated atria.
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A model of metabolic anoxia was used to investigate the modulatory effect of bradykinin (BK) on the release of noradrenaline (NA) in isolated rat atria. Atria were isolated from Wistar rats and inserted into a perfusion system. After an equilibration period of 20 min, the perfusate was collected
Analysis of the effects of graded levels of hypoxia on noradrenaline-evoked contraction in the rat iliac artery in vitro.
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In rings of rat iliac artery, contractions were evoked by noradrenaline (NA), the selective alpha(1) adrenoceptor agonist phenylephrine (PE), and K(+), which causes depolarisation-induced contraction. There was no evidence of alpha(2) adrenoceptor-evoked contraction. Hypoxia, induced by reducing
Power spectrum analysis of the fetal heart rate during noradrenaline infusion and acute hypoxemia in the chronic fetal lamb preparation.
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In a chronically instrumented fetal lamb the effect on heart rate variability of noradrenaline as well as hypoxemia is studied by the use of power spectral analysis. Subsequent to both noradrenaline infusion and hypoxemia the very low frequency components of the variability are markedly decreased as
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