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http://purl.uniprot.org/citations/26398936http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/26398936http://www.w3.org/2000/01/rdf-schema#comment"The activin receptor-like kinase 1 (ALK-1) is a type I cell-surface receptor for the transforming growth factor-β (TGF-β) family of proteins. Hypertension is related to TGF-β1, because increased TGF-β1 expression is correlated with an elevation in arterial pressure (AP) and TGF-β expression is upregulated by the renin-angiotensin-aldosterone system. The purpose of this study was to assess the role of ALK-1 in regulation of AP using Alk1 haploinsufficient mice (Alk1(+/-)). We observed that systolic and diastolic AP were significantly higher in Alk1(+/-) than in Alk1(+/+) mice, and all functional and structural cardiac parameters (echocardiography and electrocardiography) were similar in both groups. Alk1(+/-) mice showed alterations in the circadian rhythm of AP, with higher AP than Alk1(+/+) mice during most of the light period. Higher AP in Alk1(+/-) mice is not a result of a reduction in the NO-dependent vasodilator response or of overactivation of the peripheral renin-angiotensin system. However, intracerebroventricular administration of losartan had a hypotensive effect in Alk1(+/-) and not in Alk1(+/+) mice. Alk1(+/-) mice showed a greater hypotensive response to the β-adrenergic antagonist atenolol and higher concentrations of epinephrine and norepinephrine in plasma than Alk1(+/+) mice. The number of brain cholinergic neurons in the anterior basal forebrain was reduced in Alk1(+/-) mice. Thus, we concluded that the ALK-1 receptor is involved in the control of AP, and the high AP of Alk1(+/-) mice is explained mainly by the sympathetic overactivation shown by these animals, which is probably related to the decreased number of cholinergic neurons."xsd:string
http://purl.uniprot.org/citations/26398936http://purl.org/dc/terms/identifier"doi:10.1242/dmm.019695"xsd:string
http://purl.uniprot.org/citations/26398936http://purl.uniprot.org/core/author"ten Dijke P."xsd:string
http://purl.uniprot.org/citations/26398936http://purl.uniprot.org/core/author"Lopez-Novoa J.M."xsd:string
http://purl.uniprot.org/citations/26398936http://purl.uniprot.org/core/author"Perez-Barriocanal F."xsd:string
http://purl.uniprot.org/citations/26398936http://purl.uniprot.org/core/author"Pericacho M."xsd:string
http://purl.uniprot.org/citations/26398936http://purl.uniprot.org/core/author"Fuentes-Calvo I."xsd:string
http://purl.uniprot.org/citations/26398936http://purl.uniprot.org/core/author"Cruz-Gonzalez I."xsd:string
http://purl.uniprot.org/citations/26398936http://purl.uniprot.org/core/author"Oujo B."xsd:string
http://purl.uniprot.org/citations/26398936http://purl.uniprot.org/core/author"Gonzalez-Nunez M."xsd:string
http://purl.uniprot.org/citations/26398936http://purl.uniprot.org/core/author"Riolobos A.S."xsd:string
http://purl.uniprot.org/citations/26398936http://purl.uniprot.org/core/author"Castellano O."xsd:string
http://purl.uniprot.org/citations/26398936http://purl.uniprot.org/core/author"de los Angeles Sevilla M."xsd:string
http://purl.uniprot.org/citations/26398936http://purl.uniprot.org/core/date"2015"xsd:gYear
http://purl.uniprot.org/citations/26398936http://purl.uniprot.org/core/name"Dis Model Mech"xsd:string
http://purl.uniprot.org/citations/26398936http://purl.uniprot.org/core/pages"1427-1439"xsd:string
http://purl.uniprot.org/citations/26398936http://purl.uniprot.org/core/title"Heterozygous disruption of activin receptor-like kinase 1 is associated with increased arterial pressure in mice."xsd:string
http://purl.uniprot.org/citations/26398936http://purl.uniprot.org/core/volume"8"xsd:string
http://purl.uniprot.org/citations/26398936http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/26398936
http://purl.uniprot.org/citations/26398936http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/26398936
http://purl.uniprot.org/uniprot/#_D3Z7H9-mappedCitation-26398936http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/26398936
http://purl.uniprot.org/uniprot/#_D3YUY5-mappedCitation-26398936http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/26398936
http://purl.uniprot.org/uniprot/#_Q61288-mappedCitation-26398936http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/26398936
http://purl.uniprot.org/uniprot/#_Q91YV1-mappedCitation-26398936http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/26398936