| Anti-hypertensive effects of probenecid via inhibition of the α-adrenergic receptor. | |
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MedLine Citation:
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PMID: 22180356 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
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Probenecid has long been used in the treatment of gout. Its anti-gout mechanisms consist of uric acid reuptake inhibition and the consequent facilitation of uric acid excretion. In the present study, we investigated whether probenecid could exert an anti-hypertensive effect in spontaneously hypertensive rats (SHR). The noninvasive indirect tail cuff method was employed to measure blood pressure and heart rate. The administration of probenecid (50 mg/kg, ip) induced a significant systolic blood pressure (SBP) decrease, from 167 mmHg to 141 mmHg, within 120 min. In contrast, probenecid had little effect on normotensive control Wistar Kyoto rats (WKY). The anti-hypertensive effects of probenecid are almost as potent as those of atenolol. In a further exploration of the anti-hypertensive mechanisms of probenecid, its effects on phenylephrine-induced blood vessel contraction were tested. Our results suggest that probenecid significantly inhibited the contractions of rat aorta. This effect was also observed with endothelium-removed rat aorta, suggesting that probenecid can directly interact with the α-adrenergic receptor. Moreover, probenecid inhibited the α-adrenergic-receptor-mediated activation of ERK I/II in MC3TC-E1 cells. Therefore, our results indicate that probenecid might alleviate high blood pressure in SHR via inhibition of the α-adrenergic receptor and ERK I/II. |
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Authors:
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Jin Baek Park; Sung-Jin Kim |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Pharmacological reports : PR Volume: 63 ISSN: 1734-1140 ISO Abbreviation: Pharmacol Rep Publication Date: 2011 Sep |
Date Detail:
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Created Date: 2011-12-19 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 101234999 Medline TA: Pharmacol Rep Country: Poland |
Other Details:
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Languages: eng Pagination: 1145-50 Citation Subset: IM |
Affiliation:
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Department of Pharmacology and Toxicology, Metabolic Diseases Research Laboratory, School of Dentistry, Kyung Hee University, Seoul, Korea. kimsj@khu.ac.kr. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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