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http://purl.uniprot.org/citations/28717991http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/28717991http://www.w3.org/2000/01/rdf-schema#comment"Prolonged bed rest (PBR) causes orthostatic hypotension (OH). Rapid constriction of splanchnic resistance arteries in response to a sudden increase in sympathetic tone contributes to the recovery of orthostatic arterial pressure upon standing. However, the molecular mechanism of PBR-induced dysfunction in arterial constriction is not fully understood. Previously, we showed that CPI-17, a regulatory protein for myosin phosphatase, mediates α1A-adrenergic receptor-induced rapid contraction of small mesenteric arteries. Here, we tested whether PBR associated with OH affects the α1-adrenergic receptor-induced CPI-17 signaling pathway in mesenteric arteries using rats treated by head-down tail-suspension hindlimb unloading (HDU), an experimental OH model. In normal anesthetized rats, mean arterial pressure (MAP) rapidly reduced upon 90° head-up tilt from supine position and then immediately recovered without change in heart rate, suggesting a rapid arterial constriction. On the other hand, after a 4-week HDU treatment, the fast orthostatic MAP recovery failed for 1 min. Alpha1A subtype-specific antagonist suppressed the orthostatic MAP recovery with a small decrease in basal blood pressure, whereas non-specific α1-antagonist prazosin strongly reduced both basal MAP and orthostatic recovery. The HDU treatment resulted in 68% reduction in contraction in parallel with 83% reduction in CPI-17 phosphorylation in denuded mesenteric arteries 10 s after α1-agonist stimulation. The treatment with either Ca2+-release channel opener or PKC inhibitor mimicked the deficiency in HDU arteries. These results suggest that an impairment of the rapid PKC/CPI-17 signaling pathway downstream of α1A-adrenoceptors in peripheral arterial constriction, as an end organ of orthostatic blood pressure reflex, is associated with OH in prolonged bed rest patients."xsd:string
http://purl.uniprot.org/citations/28717991http://purl.org/dc/terms/identifier"doi:10.1007/s00424-017-2031-x"xsd:string
http://purl.uniprot.org/citations/28717991http://purl.uniprot.org/core/author"Kitazawa K."xsd:string
http://purl.uniprot.org/citations/28717991http://purl.uniprot.org/core/author"Kitazawa T."xsd:string
http://purl.uniprot.org/citations/28717991http://purl.uniprot.org/core/date"2017"xsd:gYear
http://purl.uniprot.org/citations/28717991http://purl.uniprot.org/core/name"Pflugers Arch"xsd:string
http://purl.uniprot.org/citations/28717991http://purl.uniprot.org/core/pages"1651-1662"xsd:string
http://purl.uniprot.org/citations/28717991http://purl.uniprot.org/core/title"Prolonged bed rest impairs rapid CPI-17 phosphorylation and contraction in rat mesenteric resistance arteries to cause orthostatic hypotension."xsd:string
http://purl.uniprot.org/citations/28717991http://purl.uniprot.org/core/volume"469"xsd:string
http://purl.uniprot.org/citations/28717991http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/28717991
http://purl.uniprot.org/citations/28717991http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/28717991
http://purl.uniprot.org/uniprot/#_A6J9Q5-mappedCitation-28717991http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/28717991
http://purl.uniprot.org/uniprot/#_Q99MC0-mappedCitation-28717991http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/28717991
http://purl.uniprot.org/uniprot/A6J9Q5http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/28717991
http://purl.uniprot.org/uniprot/Q99MC0http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/28717991