Document Detail

Mechanisms of partial renal infarct hypertension.
MedLine Citation:
PMID:  3385205     Owner:  NLM     Status:  MEDLINE    
Contributions of both the renin-angiotensin and immune systems to the aetiology of renal infarct hypertension were examined in Sprague-Dawley rats. Partial renal infarction was produced by ligating and sectioning two out of three branches of the left renal artery. The right kidney remained intact. Renal infarction resulted in rapid development of stable hypertension. One week following infarction, the plasma renin activity (PRA) increased more than threefold. However, PRA returned to control levels 4 weeks after infarction. Chronic immunosuppressive therapy with cyclophosphamide at most only attenuated the development of renal infarct hypertension associated with this transient renin elevation. However, cyclophosphamide prevented the later maintenance phase of the hypertension, and could also completely reverse established infarct hypertension. Activation of the renin-angiotensin system plays a role in the onset of partial renal infarct hypertension, but an intact immune system is required for maintenance of the hypertension. It is hypothesized that immunological reactions against renal tissue maintain renal infarct hypertension.
R A Norman; P G Galloway; D J Dzielak; M Huang
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Journal of hypertension     Volume:  6     ISSN:  0263-6352     ISO Abbreviation:  J. Hypertens.     Publication Date:  1988 May 
Date Detail:
Created Date:  1988-07-29     Completed Date:  1988-07-29     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  8306882     Medline TA:  J Hypertens     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  397-403     Citation Subset:  IM    
Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson 39216-4505.
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MeSH Terms
Cyclophosphamide / pharmacology
Hypertension, Renal / etiology*,  immunology,  physiopathology
Infarction / complications,  immunology,  physiopathology*
Kidney / blood supply*
Renin-Angiotensin System
Grant Support
Reg. No./Substance:

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