August 28, 2008AJP Renal PhysiologyOpen Access

Continuously measured renal blood flow does not increase in diabetes if nitric oxide synthesis is blocked

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Why the study?

Does blocking nitric oxide synthesis with L-NAME prevent renal vasodilation and impaired autoregulation in a rat model of type 1 diabetes?

Structured PICO

Does blocking nitric oxide synthesis with L-NAME prevent renal vasodilation and impaired autoregulation in a rat model of type 1 diabetes?

Population

Rats instrumented with artery and vein catheters and a Transonic flow probe on the left renal artery

Intervention

Streptozotocin (40 mg/kg iv) to induce diabetes plus nitro-L-arginine methyl ester (L-NAME) to block nitric oxide synthesis

Comparator

Control rats, diabetic rats without L-NAME, and control rats with L-NAME

Outcome

Renal blood flow (RBF) and arterial pressure (AP) measured 16 h/daysurrogate

Nitric oxide plays a key role in causing renal vasodilation and blunting renal blood flow autoregulation during the onset of type 1 diabetes.

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Supports nitric oxide mediation of renal vasodilation in early diabetes models; leaves open clinical translation to human autoregulation therapies.

Bell et al. (2008) studied this question.

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Supports nitric oxide mediation of renal vasodilation in early diabetes models; leaves open clinical translation to human autoregulation therapies.