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April 1, 1998AJP Renal Physiology

Downregulation of nitric oxide synthase in chronic renal insufficiency: role of excess PTH

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Why the study?

Does calcium channel blockade or parathyroidectomy improve nitric oxide synthase activity and expression in rats with chronic renal failure?

Population

Rats with chronic renal failure induced by five-sixths nephrectomy

Comparison

Felodipine treatment or parathyroidectomy (PTX) vs Sham-operated controls and untreated CRF rats

Design

Preclinical

Follow-up

6 weeks

Authors

NVNosratola D. VaziriUniversity of GenevaZNZhenmin NiXuzhou Medical CollegeXWX. Q. WangUniversity of California, Irvine

Discussion

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Implication

Calcium channel blockade or parathyroidectomy may restore vascular NOS in experimental CRF; hypothesis-generating for calcium dysregulation in uremic endothelial dysfunction.

Structured PICO

Does calcium channel blockade or parathyroidectomy improve nitric oxide synthase activity and expression in rats with chronic renal failure?

P
Population
Rats with chronic renal failure (CRF) induced by five-sixths nephrectomy (surgical resection of the upper and lower thirds of the left kidney, followed by contralateral nephrectomy)
I
Intervention
Felodipine treatment or parathyroidectomy (PTX)
C
Comparator
Sham-operated controls and untreated CRF rats
O
Outcome
Vascular nitric oxide synthase (NOS) activity and endothelial/inducible NO synthase (eNOS and iNOS) protein expressionssurrogate

In a rat model of chronic renal failure, downregulation of vascular nitric oxide synthase is reversed by calcium channel blockade or parathyroidectomy, suggesting a causal role for calcium dysregulation.

Cite This Study

Vaziri et al. (1998) studied this question.

synapsesocial.com/papers/6a72f4ebffd6abdd46748ca6https://doi.org/10.1152/ajprenal.1998.274.4.f642
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