Key result
In 2K1C hypertensive rats, L-NAME decreased renal blood flow in the nonclipped kidney by 61% (P<0.001), whereas losartan reduced blood pressure and normalized blood flow in the clipped kidney.
Why the study?
Does angiotensin II antagonism with losartan alter the renal hemodynamic response to nitric oxide synthesis inhibition in 2K1C renovascular hypertensive rats?
Population
Anesthetized two-kidney, one clip (2K1C) renovascular hypertensive rats 4 weeks after clipping (n=10)
Comparison
Nitric oxide synthesis inhibition with 10 mg/kg… vs 10 mg/kg body wt L-NAME in hypertensive rats…
Design
Preclinical
Follow-up
Acute (during anesthesia)
Authors
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Hypothesis-generating for NO-Ang II interplay in renovascular hypertension; human studies required before clinical translation.
Does angiotensin II antagonism with losartan alter the renal hemodynamic response to nitric oxide synthesis inhibition in 2K1C renovascular hypertensive rats?
The study demonstrates significant interactions between endothelium-derived nitric oxide and angiotensin II in regulating bilateral renal blood flow in renovascular hypertension.
Sigmon et al. (1993) studied Renovascular hypertension (n=10). L-NAME (with or without losartan) vs. Untreated (no losartan) was evaluated on Bilateral renal blood flow and blood pressure. In 2K1C hypertensive rats, L-NAME decreased renal blood flow in the nonclipped kidney by 61% (P<0.001), whereas losartan reduced blood pressure and normalized blood flow in the clipped kidney.
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