http://purl.uniprot.org/citations/12105146 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/12105146 | http://www.w3.org/2000/01/rdf-schema#comment | "In an attempt to elucidate whether there is a specific alpha1-adrenergic receptor (alpha1-AR) subtype involved in the genesis or maintenance of hypertension, the alpha1D-AR subtype was evaluated in a model of salt-induced hypertension. The alpha1D-AR-deficient (alpha1D-/-) and control (alpha1D+/+) mice (n=8 to 14 in each group) were submitted to subtotal nephrectomy and given 1% saline as drinking water for 35 days. Blood pressure (BP) was monitored by tail-cuff readings and confirmed at the end point by direct intraarterial BP recording. The alpha1D-/-mice had a significantly (P=0.0004) attenuated increase in BP response in this protocol (baseline 94.6+/-2.8 versus end point 107.4+/-4.5 mm Hg) compared with that of their wild-type counterparts (alpha1D+/+), from a baseline 97.4+/-2.9 to an end point 139.4+/-4.5 mm Hg. Seven of 15 alpha1D+/+ mice died with edema, probably owing to renal failure, whereas 14 of 15 alpha1D-/-mice were maintained for 35 days. Body weight, renal remnant weight, and residual renal function were similar in the 2 groups, whereas the values of plasma catecholamines (epinephrine, norepinephrine, and dopamine) were higher in alpha1D+/+ than in the alpha1D-/-mice. These data suggest that alpha1D-AR plays an important role in developing a high BP in response to dietary salt-loading, and that agents having selective alpha1D-AR antagonism could have significant therapeutic potential in the treatment of hypertension."xsd:string |
http://purl.uniprot.org/citations/12105146 | http://purl.org/dc/terms/identifier | "doi:10.1161/01.hyp.0000022062.70639.1c"xsd:string |
http://purl.uniprot.org/citations/12105146 | http://purl.uniprot.org/core/author | "Tsujimoto G."xsd:string |
http://purl.uniprot.org/citations/12105146 | http://purl.uniprot.org/core/author | "Tanoue A."xsd:string |
http://purl.uniprot.org/citations/12105146 | http://purl.uniprot.org/core/author | "Hosoda C."xsd:string |
http://purl.uniprot.org/citations/12105146 | http://purl.uniprot.org/core/author | "Koshimizu T.A."xsd:string |
http://purl.uniprot.org/citations/12105146 | http://purl.uniprot.org/core/author | "Miyawaki S."xsd:string |
http://purl.uniprot.org/citations/12105146 | http://purl.uniprot.org/core/author | "Koba M."xsd:string |
http://purl.uniprot.org/citations/12105146 | http://purl.uniprot.org/core/author | "Oshikawa S."xsd:string |
http://purl.uniprot.org/citations/12105146 | http://purl.uniprot.org/core/date | "2002"xsd:gYear |
http://purl.uniprot.org/citations/12105146 | http://purl.uniprot.org/core/name | "Hypertension"xsd:string |
http://purl.uniprot.org/citations/12105146 | http://purl.uniprot.org/core/pages | "101-106"xsd:string |
http://purl.uniprot.org/citations/12105146 | http://purl.uniprot.org/core/title | "Role of the alpha1D-adrenergic receptor in the development of salt-induced hypertension."xsd:string |
http://purl.uniprot.org/citations/12105146 | http://purl.uniprot.org/core/volume | "40"xsd:string |
http://purl.uniprot.org/citations/12105146 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/12105146 |
http://purl.uniprot.org/citations/12105146 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/12105146 |
http://purl.uniprot.org/uniprot/#_A2ANQ2-mappedCitation-12105146 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/12105146 |
http://purl.uniprot.org/uniprot/#_P97714-mappedCitation-12105146 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/12105146 |
http://purl.uniprot.org/uniprot/A2ANQ2 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/12105146 |
http://purl.uniprot.org/uniprot/P97714 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/12105146 |