Document Detail


Role of blood pressure in mediating the influence of salt intake on renin expression in the kidney.
MedLine Citation:
PMID:  22357914     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The salt intake of an organism controls the number of renin-producing cells in the kidney by yet undefined mechanisms. This study aimed to assess a possible mediator role of preglomerular blood pressure in the control of renin expression by oral salt intake. We used wild-type (WT) mice and mice lacking angiotensin II type 1a receptors (AT(1a)-/-) displaying an enhanced salt sensitivity to renin expression. In WT kidneys, we found renin-expressing cells at the ends of all afferent arterioles. A low-salt diet (0.02%) led to a moderate twofold increase in renin-expressing cells along afferent arterioles. In AT(1a)-/- mice, lowering of salt content led to a 12-fold increase in renin expression. Here, the renin-expressing cells were distributed along the preglomerular vascular tree in a typical distal-to-proximal distribution gradient which was most prominent at high salt intake and was obliterated at low salt intake by the appearance of renin-expressing cells in proximal parts of the preglomerular vasculature. While lowering of salt intake produced only a small drop in blood pressure in WT mice, the marked reduction of systolic blood pressure in AT(1a)-/- mice was accompanied by the disappearance of the distribution gradient from afferent arterioles to arcuate arteries. Unilateral renal artery stenosis in AT(1a)-/- mice on a normal salt intake produced a similar distribution pattern of renin-expressing cells as did low salt intake. Conversely, increasing blood pressure by administration of the NOS inhibitor N-nitro-l-arginine methyl ester or of the adrenergic agonist phenylephrine in AT(1a)-/- mice kept on low salt intake produced a similar distribution pattern of renin-producing cells as did normal salt intake alone. These findings suggest that changes in preglomerular blood pressure may be an important mediator of the influence of salt intake on the number and distribution of renin-producing cells in the kidney.
Authors:
Katharina Machura; Björn Neubauer; Dominik Steppan; Ramona Kettl; Andreas Groβ; Armin Kurtz
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2012-02-22
Journal Detail:
Title:  American journal of physiology. Renal physiology     Volume:  302     ISSN:  1522-1466     ISO Abbreviation:  Am. J. Physiol. Renal Physiol.     Publication Date:  2012 May 
Date Detail:
Created Date:  2012-05-16     Completed Date:  2012-07-18     Revised Date:  2012-10-03    
Medline Journal Info:
Nlm Unique ID:  100901990     Medline TA:  Am J Physiol Renal Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  F1278-85     Citation Subset:  IM    
Affiliation:
Physiologisches Institut, Universität Regensburg, D-93053 Regensburg, Germany. katharina.machura@vkl.uni-regensburg.de
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MeSH Terms
Descriptor/Qualifier:
Adrenergic alpha-1 Receptor Agonists / pharmacology
Animals
Arterioles / physiology
Blood Pressure / drug effects,  physiology*
Enzyme Inhibitors / pharmacology
Homeostasis / physiology
Juxtaglomerular Apparatus / physiology
Kidney / blood supply,  physiology*
Mice
Mice, 129 Strain
Mice, Knockout
NG-Nitroarginine Methyl Ester / pharmacology
Phenylephrine / pharmacology
Receptor, Angiotensin, Type 1 / genetics*,  metabolism
Renin / genetics*,  metabolism
Sodium Chloride, Dietary / pharmacology*
Chemical
Reg. No./Substance:
0/Adrenergic alpha-1 Receptor Agonists; 0/Enzyme Inhibitors; 0/Receptor, Angiotensin, Type 1; 0/Sodium Chloride, Dietary; 50903-99-6/NG-Nitroarginine Methyl Ester; 59-42-7/Phenylephrine; EC 3.4.23.15/Renin

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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