Document Detail

Cosegregation of the renin allele of the spontaneously hypertensive rat with an increase in blood pressure.
MedLine Citation:
PMID:  1969424     Owner:  NLM     Status:  MEDLINE    
The spontaneously hypertensive rat (SHR) exhibits alterations in the renin-angiotensin-aldosterone system which are similar to those that characterize patients with "nonmodulating" hypertension, a common and highly heritable form of essential hypertension. Accordingly, we determined whether the inheritance of a DNA restriction fragment length polymorphism (RFLP) marking the renin gene of the SHR was associated with greater blood pressure than inheritance of a RFLP marking the renin gene of a normotensive control rat. In an F2 population derived from inbred SHR and inbred normotensive Lewis rats, we found the blood pressure in rats that inherited a single SHR renin allele to be significantly greater than that in rats that inherited only the Lewis renin allele. To the extent that the SHR provides a suitable model of "nonmodulating" hypertension, these findings raise the possibility that a structural alteration in the renin gene, or a closely linked gene, may be a pathogenetic determinant of increased blood pressure in one of the most common forms of essential hypertension in humans.
T W Kurtz; L Simonet; P M Kabra; S Wolfe; L Chan; B L Hjelle
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The Journal of clinical investigation     Volume:  85     ISSN:  0021-9738     ISO Abbreviation:  J. Clin. Invest.     Publication Date:  1990 Apr 
Date Detail:
Created Date:  1990-05-09     Completed Date:  1990-05-09     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  7802877     Medline TA:  J Clin Invest     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1328-32     Citation Subset:  AIM; IM    
Department of Laboratory Medicine, University of California, San Francisco 94143.
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MeSH Terms
Amino Acid Sequence
Blood Pressure*
Hypertension / etiology*,  genetics
Polymorphism, Restriction Fragment Length
Rats, Inbred Lew
Rats, Inbred SHR
Renin / genetics*
Grant Support
Reg. No./Substance:

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