Document Detail


Endothelin type a receptor blockade attenuates the hypertension in response to chronic reductions in uterine perfusion pressure.
MedLine Citation:
PMID:  11230323     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
A chronic reduction in uterine perfusion pressure in pregnant rats is associated with a significant elevation in mean arterial pressure (MAP) and reduction in kidney function. The purpose of this study was to examine the role of endothelin in mediating the hypertension in response to chronic reductions in uterine perfusion pressure in conscious, chronically instrumented, pregnant rats. MAP in pregnant rats with chronic reductions in uterine perfusion pressure (123.0+/-1.8 mm Hg) was significantly higher than that in control pregnant rats (101.3+/-4.0 mm Hg). Renal expression of preproendothelin mRNA as determined by ribonuclease protection assay was also significantly elevated in the medulla (>45%, P<0.05) and in the cortex (>22%, P:<0.05) of the pregnant rats with chronic reductions in uterine perfusion pressure compared with control pregnant rats. Chronic administration of the selective endothelin type A receptor antagonist (ABT-627, 5 mg/kg per day for 10 days) markedly attenuated the increase in MAP observed in the pregnant rats with chronic reductions in uterine perfusion pressure (103.3+/-5.6 mm Hg, plus endothelin antagonist; P<0.05). However, endothelin type A receptor blockade had no significant effect on blood pressure in the normal pregnant animals (96.0+/-2.7 mm Hg, plus endothelin antagonist). These findings suggest that endothelin plays a major role in mediating the hypertension produced by chronic reductions in uterine perfusion pressure in pregnant rats.
Authors:
B T Alexander; A N Rinewalt; K L Cockrell; M B Massey; W A Bennett; J P Granger
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Hypertension     Volume:  37     ISSN:  1524-4563     ISO Abbreviation:  Hypertension     Publication Date:  2001 Feb 
Date Detail:
Created Date:  2001-03-20     Completed Date:  2001-04-26     Revised Date:  2013-03-18    
Medline Journal Info:
Nlm Unique ID:  7906255     Medline TA:  Hypertension     Country:  United States    
Other Details:
Languages:  eng     Pagination:  485-9     Citation Subset:  IM    
Affiliation:
Departments of Physiology and Obstetrics and Gynecology, Center for Excellence in Cardiovascular-Renal Research Center, University of Mississippi Medical Center, Jackson, MS, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Blood Pressure / drug effects
Endothelin-1
Endothelins / antagonists & inhibitors,  metabolism,  pharmacology,  physiology*
Female
Hypertension / physiopathology*
Kidney Cortex / metabolism
Kidney Medulla / metabolism
Perfusion
Pregnancy
Pregnancy Complications, Cardiovascular / physiopathology*
Protein Precursors / metabolism
Pyrrolidines / pharmacology
RNA, Messenger / isolation & purification,  metabolism
Rats
Receptor, Endothelin A
Receptors, Endothelin / antagonists & inhibitors*
Uterus / blood supply*,  physiology
Grant Support
ID/Acronym/Agency:
HL-10137-01/HL/NHLBI NIH HHS; HL-38499/HL/NHLBI NIH HHS; HL-51971/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/A 127722; 0/Endothelin-1; 0/Endothelins; 0/Protein Precursors; 0/Pyrrolidines; 0/RNA, Messenger; 0/Receptor, Endothelin A; 0/Receptors, Endothelin

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


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