Early-onset endothelin receptor blockade in hypertensive heterozygous Ren-2 rats
Language English Country United States Media print-electronic
Document type Comparative Study, Journal Article, Research Support, Non-U.S. Gov't
PubMed
16807127
DOI
10.1016/j.vph.2006.05.003
PII: S1537-1891(06)00117-0
Knihovny.cz E-resources
- MeSH
- Endothelin A Receptor Antagonists MeSH
- Endothelin B Receptor Antagonists MeSH
- Endothelin Receptor Antagonists * MeSH
- Antihypertensive Agents pharmacology therapeutic use MeSH
- Atrasentan MeSH
- Bosentan MeSH
- Time Factors MeSH
- Endothelin-1 metabolism MeSH
- Glomerulosclerosis, Focal Segmental prevention & control MeSH
- Animals, Genetically Modified MeSH
- Heterozygote MeSH
- Hypertension chemically induced metabolism physiopathology prevention & control MeSH
- Cardiomegaly prevention & control MeSH
- Blood Pressure drug effects MeSH
- Rats MeSH
- Sodium Chloride, Dietary MeSH
- Disease Models, Animal MeSH
- Rats, Sprague-Dawley MeSH
- Proteinuria prevention & control MeSH
- Pyrrolidines pharmacology therapeutic use MeSH
- Receptors, Endothelin metabolism MeSH
- Renin genetics MeSH
- Sulfonamides pharmacology therapeutic use MeSH
- Body Weight drug effects MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Comparative Study MeSH
- Names of Substances
- Endothelin A Receptor Antagonists MeSH
- Endothelin B Receptor Antagonists MeSH
- Endothelin Receptor Antagonists * MeSH
- Antihypertensive Agents MeSH
- Atrasentan MeSH
- Bosentan MeSH
- Endothelin-1 MeSH
- Sodium Chloride, Dietary MeSH
- Pyrrolidines MeSH
- Receptors, Endothelin MeSH
- Ren2 protein, mouse MeSH Browser
- Renin MeSH
- Sulfonamides MeSH
Male heterozygous Ren-2 transgenic rats and Hannover Sprague-Dawley rats fed a normal or high-salt diet were either untreated or treated with the nonselective receptor ET(A)/ET(B) receptor blocker bosentan or the selective ET(A) receptor blocker, ABT-627, known as atrasentan. Survival rate was partly increased by bosentan and fully normalized by atrasentan. Bosentan did not significantly influence the course of hypertension in TGR, whereas atrasentan significantly decreased BP on both diets. Atrasentan substantially reduced proteinuria, cardiac hypertrophy, glomerulosclerosis and left ventricular ET-1 tissue concentration on both diets. Our data indicate that ET(A) receptor blockade is superior to nonselective blockade in attenuating hypertension, end-organ damage and improving survival rate.
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