Document Detail

Angiotensin II causes vascular hypertrophy in part by a non-pressor mechanism.
MedLine Citation:
PMID:  2022407     Owner:  NLM     Status:  MEDLINE    
Angiotensin II, when given in low doses, raises blood pressure slowly. When tested in vitro on vascular smooth muscle cells, it has mitogenic and trophic effects; it is not known if it has these effects in vivo. Our purpose was to determine whether vascular hypertrophy develops during slow pressor infusion of angiotensin II and, if so, whether it is pressure induced. Three experiments were done in rats infused subcutaneously with angiotensin II (200 ng/kg/min) by minipump for 10-12 days. Experiment 1: Angiotensin II gradually raised systolic blood pressure (measured in the tail) from 143 +/- 2 to 208 +/- 8 mm Hg (mean +/- SEM), significantly suppressing plasma renin and increasing threefold (NS) plasma angiotensin II. There was no loss of peptide in the pump infusate when tested at the end of the experiment. Experiment 2: In the perfused mesenteric circulation, vasoconstrictor responses to norepinephrine, vasopressin, and KCl were enhanced in rats given a slow pressor infusion of angiotensin II, but sensitivity of responses was not altered. This combination of changes suggests that vascular hypertrophy develops during slow pressor infusion of angiotensin II. Experiment 3: Vessel myography was done after angiotensin II infusion with and without a pressor response. Angiotensin II raised systolic blood pressure, increased heart weight, and produced myographic changes of vascular hypertrophy in the mesenteric circulation, increasing media width, media cross-sectional area, and media/lumen ratio. Hydralazine given with angiotensin II prevented the rise of pressure and the cardiac effect but not the vascular changes. Two-way analysis of variance showed that angiotensin II significantly increased media width, media cross-sectional area, and media/lumen ratio, all independent of hydralazine. Thus, although hydralazine inhibits the pressor and cardiac effects of angiotensin II, suggesting a pressor mechanism for the cardiac change, it does not inhibit structural vascular change, which suggests that at least part of the effect has a non-pressor mechanism.
S A Griffin; W C Brown; F MacPherson; J C McGrath; V G Wilson; N Korsgaard; M J Mulvany; A F Lever
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Hypertension     Volume:  17     ISSN:  0194-911X     ISO Abbreviation:  Hypertension     Publication Date:  1991 May 
Date Detail:
Created Date:  1991-06-06     Completed Date:  1991-06-06     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  7906255     Medline TA:  Hypertension     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  626-35     Citation Subset:  IM    
MRC Blood Pressure Unit, Western Infirmary, Glasgow, Scotland.
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MeSH Terms
Angiotensin II / blood,  pharmacology*
Blood Pressure / drug effects
Blood Vessels / drug effects*,  pathology
Infusion Pumps
Injections, Subcutaneous
Rats, Inbred Strains
Renin / blood
Splanchnic Circulation / drug effects
Reg. No./Substance:
11128-99-7/Angiotensin II; EC

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