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AT1 receptor blockade improves vasorelaxation in experimental renal failure
Peeter Kööbi1, Jarkko Kalliovalkama, Pasi Jolma
1Department of Pharmacological Sciences, University of Tampere, Finland.
Hypertension (Dallas, Tex. : 1979)
|May 14, 2003
Summary
Losartan therapy normalized small artery function and structure in rats with renal failure. This angiotensin II receptor antagonist improved vasodilation and reversed harmful arterial remodeling, independent of blood pressure changes.
Area of Science:
- Cardiovascular Physiology
- Renal Physiology
- Pharmacology
Background:
- Renal failure is associated with impaired small artery function and morphology.
- The role of angiotensin II type 1 receptor antagonists in modulating these vascular changes is not well understood.
Purpose of the Study:
- To investigate the effects of losartan, an angiotensin II type 1 receptor antagonist, on the function and morphology of mesenteric resistance arteries in a rat model of renal failure.
Main Methods:
- Utilized 5/6 nephrectomized rats treated with losartan for 8 weeks.
- Assessed arterial function using wire and pressure myography.
- Analyzed arterial morphology and aortic angiotensin-converting enzyme (ACE) content.
Main Results:
- Nephrectomized rats exhibited impaired endothelium-dependent and independent vasodilation and eutrophic inward remodeling of resistance arteries.
- Losartan therapy normalized arterial relaxation and morphology.
- Aortic ACE content correlated with plasma urea nitrogen, suggesting enhanced vascular renin-angiotensin system activity in renal failure.
Conclusions:
- Losartan effectively normalized resistance artery function and morphology in experimental renal failure.
- These beneficial effects were independent of blood pressure changes, kidney function, or volume overload.
- Improved vasodilation may involve enhanced relaxation via potassium channels.