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5/6th Nephrectomy in Combination with High Salt Diet and Nitric Oxide Synthase Inhibition to Induce Chronic Kidney Disease in the Lewis Rat
Published on: July 3, 2013
Vascular function in rats with adenine-induced chronic renal failure
Lisa Nguy1, Holger Nilsson, Jaana Lundgren
1Department of Molecular and Clinical Medicine/Nephrology, Institute of Medicine, Sahlgrenska Academy at University of Gothenburg, Sweden. lisa.nguy@gu.se
Summary
Chronic renal failure in rats significantly impairs aortic relaxation and contraction rates, despite normal blood pressure responses to common vasoactive agents. This study reveals key vascular dysfunction in severe kidney disease.
Area of Science:
- Cardiovascular Physiology
- Nephrology
- Vascular Biology
Background:
- Chronic renal failure (CRF) is associated with cardiovascular complications.
- Adenine-induced CRF (A-CRF) in rats mimics aspects of human kidney disease.
- Vascular function in resistance arteries and the aorta during A-CRF requires detailed characterization.
Purpose of the Study:
- To investigate the functional changes in mesenteric arteries and the aorta in rats with adenine-induced chronic renal failure (A-CRF).
- To assess the impact of A-CRF on vascular responses to vasoactive agents and mechanical stimuli.
- To examine the structural alterations in the aorta associated with A-CRF.
Main Methods:
- Induction of A-CRF in Sprague-Dawley rats via adenine supplementation in chow.
- Ex vivo wire myography of mesenteric arteries and thoracic aortas.
- Measurement of plasma creatinine, blood pressure, and biochemical markers (anemia, hyperphosphatemia, hyperparathyroidism, asymmetric dimethylarginine, oxidative stress).
- Assessment of vascular sensitivity and maximal responses to acetylcholine, sodium nitroprusside, norepinephrine, and phenylephrine.
Main Results:
- A-CRF rats exhibited significantly elevated plasma creatinine, blood pressure, anemia, hyperphosphatemia, hyperparathyroidism, and increased asymmetric dimethylarginine and oxidative stress markers.
- No significant differences in sensitivity or maximal responses to vasoactive agents were observed between A-CRF and control groups.
- A-CRF significantly reduced the rate of aortic relaxation after KCl washout and in response to acetylcholine and sodium nitroprusside.
- The rate of contraction in response to KCl was also significantly reduced in both mesenteric arteries and aortas of A-CRF rats.
- A-CRF aortas showed media thickening, fragmented elastic lamellae, and disorganized smooth muscle cells, without vascular calcification.
Conclusions:
- Severe renal failure in this rat model primarily affects aortic function, notably slowing the rate of relaxation.
- The study highlights significant alterations in vascular mechanics and structure in the aorta during chronic renal failure.
- These findings suggest that CRF-induced vascular dysfunction may precede significant changes in vascular reactivity to common vasoactive stimuli.
