What is the clinical evidence from this study?

Population: Diabetes (n=42). Intervention: S-methyl-L-thiocitrulline (SMTC) vs. Baseline and normoglycemic control rats. Primary outcome: Renal oxygen consumption (QO2) and electrolyte transport efficiency (TNa/QO2) (p=<0.05).

November 19, 2009AJP Renal PhysiologyOpen Access

Nitric oxide originating from NOS1 controls oxygen utilization and electrolyte transport efficiency in the diabetic kidney

Q: What are the key findings of this study?

Selective NOS1 inhibition increased oxygen consumption and reduced electrolyte transport efficiency in the diabetic rat kidney, indicating NOS1-derived nitric oxide controls tissue oxygenation.

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Key result

Selective NOS1 inhibition increased oxygen consumption and reduced electrolyte transport efficiency in the diabetic rat kidney, indicating NOS1-derived nitric oxide controls tissue oxygenation.

Population

Age-matched male Wistar-Furth rats weighing 250-330 g, divided into streptozotocin-induced diabetic rats and…

Comparison

Selective NOS1 inhibitor S-methyl-L-thiocitrullin… vs Baseline measurements before administration of…

Design

Preclinical

Follow-up

Acute in vivo measurements

Authors

FPFredrik PalmUppsala University AFAngelica FaschingUppsala University PHPeter HansellUppsala University

Discussion

Member takes

Implication

Caution against clinical use of NOS1 inhibitors in diabetic kidney disease; leaves open therapeutic relevance pending human studies.

Structured PICO

Population

42 male Wistar-Furth rats (22 with streptozotocin-induced diabetes and 20 normoglycemic controls) were studied to evaluate the effects of selective NOS1 inhibition on renal oxygen utilization.

Intervention

Selective NOS1 inhibitor S-methyl-L-thiocitrulline (SMTC) (1 mg/kg bolus + 1 mg/kg/h continuous infusion) or nonselective NOS inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) (10 mg/kg bolus + 10 mg/kg/h continuous infusion).

Comparator

Baseline measurements before administration of the inhibitors, and comparison between control and diabetic rats.

Outcome

Oxygen utilization (QO2), electrolyte transport efficiency (TNa/QO2), renal blood flow (RBF), glomerular filtration rate (GFR), and mean arterial pressure (MAP).surrogate

Main Result

p-value: p=<0.05

Selective NOS1 inhibition increases oxygen consumption and reduces electrolyte transport efficiency in the diabetic rat kidney, indicating that NOS1-derived NO plays a pivotal role in controlling tissue oxygenation in diabetes.

Limitations

Strain differences (Wistar-Furth vs. Sprague-Dawley rats) may explain discrepancies with previous reports.
GFR can be regulated by mechanisms dissociated from direct hemodynamic effects which were not investigated.
Strain differences (Wistar-Furth vs. Sprague-Dawley rats) might explain discrepancies with previous reports regarding the effects of SMTC on MAP and RBF.

Cite This Study

Palm et al. (2009) studied Diabetes (n=42). S-methyl-L-thiocitrulline (SMTC) vs. Baseline and normoglycemic control rats was evaluated on Renal oxygen consumption (QO2) and electrolyte transport efficiency (TNa/QO2) (p=<0.05). Selective NOS1 inhibition increased oxygen consumption and reduced electrolyte transport efficiency in the diabetic rat kidney, indicating NOS1-derived nitric oxide controls tissue oxygenation.

synapsesocial.com/papers/6a71d411ac440176ef2a5dd1 https://doi.org/10.1152/ajprenal.00229.2009

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Nitric oxide originating from NOS1 controls oxygen utilization and electrolyte transport efficiency in the diabetic kidney

Discussion

Member takes

Implication

Structured PICO

Main Result

Limitations

Cite This Study

Nitric oxide originating from NOS1 controls oxygen utilization and electrolyte transport efficiency in the diabetic kidney

Discussion

Member takes

Implication

Structured PICO

Main Result

Limitations

Cite This Study

Also Consider

Also Consider