Key result
Intratubular infusion of the nitric oxide synthase inhibitor L-NNA increased tubuloglomerular feedback sensitivity and reactivity, decreasing the turning point from 19.8 to 15.2 nl/min.
Why the study?
Does intratubular infusion of L-NNA alter tubuloglomerular feedback sensitivity and reactivity in anesthetized rats?
Population
Anesthetized rats
Comparison
Intratubular infusion of nitric oxide synthase… vs Control (baseline/vehicle)
Design
Preclinical
Authors
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Supports nitric oxide attenuation of tubuloglomerular feedback in rats; leaves open translation to human glomerular hemodynamics.
Does intratubular infusion of L-NNA alter tubuloglomerular feedback sensitivity and reactivity in anesthetized rats?
Locally produced nitric oxide decreases the sensitivity of the tubuloglomerular feedback mechanism and regulates glomerular capillary pressure in rats.
Thorup et al. (1994) studied Tubuloglomerular feedback mechanism. L-NNA (N omega-nitro-L-arginine) vs. Control was evaluated on Tubuloglomerular feedback sensitivity and reactivity (turning point and delta Psf). Intratubular infusion of the nitric oxide synthase inhibitor L-NNA increased tubuloglomerular feedback sensitivity and reactivity, decreasing the turning point from 19.8 to 15.2 nl/min.
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