Document Detail


Central nervous system action of angiotensin during onset of renal hypertension in awake rats.
MedLine Citation:
PMID:  6476129     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The increase in arterial pressure and vascular resistance during acute unilateral renal artery stenosis (RSt) in conscious rats is, in part, dependent on elevated neurogenic vascular tone produced by an indirect neural interaction of angiotensin II (ANG II) with the sympathetic nervous system. The present experiments examined whether this interaction occurs within the central nervous system. Conscious rats that had been chronically instrumented with miniaturized Doppler flow probes for measurement of regional vascular resistance were subjected to a 50% reduction in unilateral renal flow with an implanted pneumatic occluder. Arterial pressure increased by 35% after 60 min of RSt. In animals in which the pressor response to intracerebroventricular (icv) ANG II had been eliminated by prior surgical interruption of the "ANG II pressor pathway" in the anterior hypothalamus, the increase in blood pressure following RSt was attenuated by 44% (P less than 0.01). In a second series, a central action of ANG II during acute renal hypertension (RH) was assessed by central ANG II receptor blockade with icv saralasin. Unlike normotensive controls, acutely RH animals responded to saralasin with significant (P less than 0.01) decreases in arterial pressure (-32%) and hindquarters (-26%) and contralateral renal (-9%) resistance. These changes were accentuated (-57% decrease in pressure) in animals made areflexic by prior sinoaortic baroreceptor denervation. Thus activation of the sympathetic nervous system during the early high-renin phase of RH depends significantly on a central action of ANG II. This mechanism may account for some 40-50% of the pressure increase following acute RSt.
Authors:
J E Faber; M J Brody
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The American journal of physiology     Volume:  247     ISSN:  0002-9513     ISO Abbreviation:  Am. J. Physiol.     Publication Date:  1984 Sep 
Date Detail:
Created Date:  1984-10-24     Completed Date:  1984-10-24     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0370511     Medline TA:  Am J Physiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  H349-60     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Afferent Pathways / physiopathology
Angiotensin II / physiology*
Animals
Carotid Sinus / physiopathology
Central Nervous System / physiopathology*
Consciousness
Constriction, Pathologic
Hypertension, Renal / physiopathology*
Hypothalamus / physiopathology
Male
Nerve Block
Pressoreceptors / physiopathology
Rats
Rats, Inbred Strains
Receptors, Angiotensin / drug effects
Reflex / physiology
Renal Artery Obstruction / physiopathology
Saralasin / pharmacology
Grant Support
ID/Acronym/Agency:
HL-06597/HL/NHLBI NIH HHS; HL-07121/HL/NHLBI NIH HHS; HL-30971/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Receptors, Angiotensin; 11128-99-7/Angiotensin II; 34273-10-4/Saralasin

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


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