| Renal Medullary Endothelin-1 is Decreased in Dahl Salt Sensitive Rats. | |
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MedLine Citation:
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PMID: 21613578 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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Although it is well established that the renal endothelin (ET-1) system plays an important role in regulating sodium excretion and blood pressure through activation of renal medullary ET-B receptors, the role of this system in Dahl salt sensitive (DS) hypertension is unclear. The purpose of this study was to determine if the DS rat has abnormalities in the renal medullary endothelin system when maintained on a high sodium intake. The data indicates that Dahl salt resistant rats (DR) on a high salt diet had a 6-fold higher urinary endothelin excretion than in the DR rats on a low Na(+) intake (17.8±4 pg/day versus 112±44 pg/day). In sharp contrast, urinary endothelin levels increased only 2 fold in DS rats in response to a high Na(+) intake (13±2 pg/day vs. 29.8±5.5 pg/day). Medullary endothelin concentration in DS rats on a high Na(+) diet was also significantly lower than DR rats on a high Na(+) intake (31 ± 2.8 pg/mg versus 70.9±5 pg/mg). Furthermore, DS rats had a significant reduction in medullary ET-B receptor expression as compared to DR rats while on a high Na(+) intake. Finally, chronic infusion of ET-1 directly into the renal medulla blunted Dahl salt-sensitive hypertension. These data indicate that a decrease in medullary production of ET-1 in the DS rat could play an important role in the development of salt sensitive hypertension observed in the DS rat. |
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Authors:
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Joshua S Speed; Babbette Lamarca; Hunter Berry; Kathy Cockrell; Eric M George; Joey P Granger |
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Publication Detail:
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Type: JOURNAL ARTICLE Date: 2011-5-25 |
Journal Detail:
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Title: American journal of physiology. Regulatory, integrative and comparative physiology Volume: - ISSN: 1522-1490 ISO Abbreviation: - Publication Date: 2011 May |
Date Detail:
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Created Date: 2011-5-26 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 100901230 Medline TA: Am J Physiol Regul Integr Comp Physiol Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Affiliation:
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1University of Mississippi Medical Center. |
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