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1 Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, Ohio 44106; 2 National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892; 3 Department of Comparative BioSciences, School of Veterinary Medicine, University of Wisconsin, Madison, Wisconsin 53706; and 4 Division of Respiratory, Critical Care, and Environmental Medicine, Department of Medicine, University of Louisville, Louisville, Kentucky 40292
This symposium was organized to present research dealing with the effects of intermittent hypoxia on cardiorespiratory systems and cellular mechanisms. The pattern of neural impulse activity has been shown to be critical in the induction of genes in neuronal cells and involves distinct signaling pathways. Mechanisms associated with different patterns of intermittent hypoxia might share similar mechanisms. Chronic intermittent hypoxia selectively augments carotid body sensitivity to hypoxia and causes long-lasting activation of sensory discharge. Intermittent hypoxia also activates hypoxia-inducible factor-1. Reactive oxygen species are critical in altering carotid body function and hypoxia-inducible factor-1 activation caused by intermittent hypoxia. Blockade of serotonin function in the spinal cord prevents long-term facilitation in respiratory motor output elicited by episodic hypoxia and requires de novo protein synthesis. Chronic intermittent hypoxia leads to sustained elevation in arterial blood pressure and is associated with upregulation of catecholaminergic and renin-angiotensin systems and downregulation of nitric oxide synthases.
protein kinases; gene expression; carotid body chemoreceptors; respiratory plasticity; blood pressure control
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