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Na+ pump inhibition and non-selective cation channel activation by cyanide and anoxia in guinea-pig chromaffin cells.
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1. Hypoxia and metabolic inhibition with cyanide (CN) evoke catecholamine secretion in adrenal chromaffin cells through depolarization. We elucidated mechanisms for a CN- or anoxia-induced inward (depolarization) current, using the perforated patch method. 2. Bath application of Ba2+ induced a
Effects of hypoxia and putative transmitters on [Ca2+]i of rat glomus cells.
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Dissociated rat glomus cells were loaded with Fura-2 AM to study the effects of hypoxia, and carotid body transmitters on intracellular calcium, [Ca2+]i. The mean control [Ca2+]i was 55 nM in isolated cells and 67 nM in clusters. The following procedures changed [Ca2+]i:0[Ca2+]o+EGTA reduced [Ca2+]i
Hypoxia and cyanide induce depolarization and catecholamine release in dispersed guinea-pig chromaffin cells.
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1. The perforated patch method and amperometry were used to determine whether the adrenal medullary cell itself is capable of sensing hypoxia and, if so, how such sensation is transduced to secretion of catecholamines (CA). 2. Exposure to hypoxia, cyanide (CN), or muscarine facilitated CA secretion
[Acute neurotoxic organophosphate poisoning: insecticides and chemical weapons].
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OBJECTIVE
To review clinical and therapeutic bases of an organophosphate poisoning, either with insecticide or nerve agent.
METHODS
References were obtained from computerized bibliographic research (Medline), from personal data (academic memoir, documents under approbation of the National Defense
[Study on the functional development of the sympathetic nervous system of fetal heart in rats].
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The drugs acting on the autonomic nervous system were administered intravenously to dams or intraperitoneally to the 20-day-old fetuses maintained by umbilical and placental circulation. The fetal heart rates were accelerated by the administration of isoproterenol, epinephrine, norepinephrine,
Muscarinic modulation of TASK-like background potassium channel in rat carotid body chemoreceptor cells.
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The carotid body is the main peripheral arterial chemoreceptor and it is essential to initiate the cardiovascular and respiratory compensatory reflex responses to a decrease in the arterial oxygen. The carotid body chemoreceptor (type-I) cells respond to hypoxia with membrane depolarization,
Hypoxic enhancement of evoked noradrenaline release from the human neuroblastoma SH-SY5Y.
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The effects of chronic hypoxia (2.5% O(2), 24 h) on [3H]noradrenaline ([3H]NA) release evoked from human neuroblastoma SH-SY5Y cells by depolarisation and by activation of muscarinic receptors was investigated. Depolarization of cells with 100 mM K(+) evoked [3H]NA release, and chronic hypoxia
Paracrine Signaling in Glial-Like Type II Cells of the Rat Carotid Body.
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The carotid body (CB) chemosensory complex uses ATP as a key excitatory neurotransmitter that is the main contributor to the sensory discharge during acute hypoxia. The complex includes receptor type I cells, which depolarize and release various neurochemicals including ATP during hypoxia, and
Cardio-ventilatory control in rainbow trout: I. Pharmacology of branchial, oxygen-sensitive chemoreceptors.
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The effects of various neurochemicals on O2-sensitive chemoreceptor afferent discharge in the glossopharyngeal nerve (cranial nerve IX) were examined in an isolated, perfused first gill arch preparation from rainbow trout. Afferent neural activity from O2 receptors in the first gill arch increased
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