| Altered whole kidney blood flow autoregulation in a mouse model of reduced beta-ENaC. | |
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MedLine Citation:
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PMID: 19889952 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Renal blood flow (RBF) autoregulation is mediated by at least two mechanisms, the fast acting myogenic response (approximately 5 s) and slow acting tubuloglomerular feedback (TGF; approximately 25 s). Previous studies suggest epithelial Na(+) channel (ENaC) family proteins, beta-ENaC in particular, mediate myogenic constriction in isolated renal interlobar arteries. However, it is unknown whether beta-ENaC-mediated myogenic constriction contributes to RBF autoregulation in vivo. Therefore, the goal of this investigation was to determine whether the myogenic mediated RBF autoregulation is inhibited in a mouse model of reduced beta-ENaC (m/m). To address this goal, we evaluated the temporal response of RBF and renal vascular resistance (RVR) to a 2-min step increase in mean arterial pressure (MAP). Pressure-induced changes in RBF and RVR at 0-5, 6-25, and 110-120 s after step increase in MAP were used to assess the contribution of myogenic and TGF mechanisms and steady-state autoregulation, respectively. The rate of the initial increase in RVR, attributed to the myogenic mechanism, was reduced by approximately 50% in m/m mice, indicating the speed of the myogenic response was inhibited. Steady-state autoregulation was similar between beta-ENaC +/+ and m/m mice. Although the rate of the secondary increase in RVR, attributed to TGF, was similar in beta-ENaC +/+ and m/m mice, however, it occurred over a longer period (+10 s), which may have allowed TGF to compensate for a loss in myogenic autoregulation. Our findings suggest beta-ENaC is an important mediator of renal myogenic constriction-mediated RBF autoregulation in vivo. |
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Authors:
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Samira C Grifoni; Rumbidzayi Chiposi; Susan E McKey; Michael J Ryan; Heather A Drummond |
Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2009-11-04 |
Journal Detail:
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Title: American journal of physiology. Renal physiology Volume: 298 ISSN: 1522-1466 ISO Abbreviation: Am. J. Physiol. Renal Physiol. Publication Date: 2010 Feb |
Date Detail:
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Created Date: 2010-01-27 Completed Date: 2010-03-09 Revised Date: 2011-07-22 |
Medline Journal Info:
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Nlm Unique ID: 100901990 Medline TA: Am J Physiol Renal Physiol Country: United States |
Other Details:
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Languages: eng Pagination: F285-92 Citation Subset: IM |
Affiliation:
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Department of Physiology and Biophysics and the Center for Excellence in Cardiovascular-Renal Research, University of Mississippi Medical Center, Jackson, Mississippi 39216-4505, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adaptation, Physiological Animals Blood Pressure / physiology Down-Regulation Epithelial Sodium Channel / metabolism* Feedback, Physiological Hemodynamics Homeostasis* Kidney Glomerulus / physiology Kidney Tubules / physiology Mice Mice, Mutant Strains Muscle, Smooth, Vascular / physiology Renal Circulation / physiology* Time Factors Vascular Resistance / physiology |
| Grant Support | |
ID/Acronym/Agency:
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HL-086996/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Epithelial Sodium Channel |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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