What question did this study set out to answer?

To determine whether intraluminal flow modulates pressure-induced myogenic constriction in glomerular afferent arterioles via endothelial release of nitric oxide or prostaglandins.

June 1, 1995Journal of Clinical InvestigationOpen Access

Flow modulates myogenic responses in isolated microperfused rabbit afferent arterioles via endothelium-derived nitric oxide.

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To determine whether intraluminal flow modulates pressure-induced myogenic constriction in glomerular afferent arterioles via endothelial release of nitric oxide or prostaglandins.
Microdissected and simultaneously perfused paired rabbit afferent arterioles, occluding one efferent arteriole with an albumin-containing perfusate to establish concurrent free-flow and no-flow conditions.
Measured arteriolar luminal diameters during stepwise pressure increments from 30 to 120 mmHg under control conditions, after endothelial disruption, and during pharmacological inhibition with L-NAME or indomethacin.
Pressure-induced constriction was significantly blunted in free-flow compared to no-flow afferent arterioles, showing luminal diameter reductions of 11.1 ± 1.7% versus 25.6 ± 2.3% (n = 30) at 120 mmHg.
Endothelial denudation and nitric oxide synthase inhibition with L-NAME selectively enhanced constriction in free-flow arterioles, completely eliminating the difference between flow states.
Cyclooxygenase inhibition with indomethacin produced no detectable changes in pressure-induced constriction in either free-flow or no-flow arterioles.

Structured PICO

Population

Isolated microperfused rabbit afferent arterioles (n=30)

Intervention

Intraluminal flow (free-flow condition) during stepwise 30-mmHg increases in intraluminal pressure (from 30 to 120 mmHg), tested before and after endothelial disruption, L-NAME, or indomethacin

Comparator

No-flow condition (occluded efferent arteriole)

Outcome

Pressure-induced constriction (luminal diameter decrease)surrogate

Intraluminal flow attenuates pressure-induced constriction in afferent arterioles via endothelium-derived nitric oxide, suggesting flow-stimulated NO release is important for controlling glomerular hemodynamics.

Discussion

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Implication

Flow-mediated NO may regulate glomerular hemodynamics in rodents; hypothesis-generating and leaves open translation to human renal autoregulation.

Cite This Study

Juncos et al. (1995) studied this question.

synapsesocial.com/papers/6a7041dae71d69abee087b8a https://doi.org/10.1172/jci117977

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Implication

Flow-mediated NO may regulate glomerular hemodynamics in rodents; hypothesis-generating and leaves open translation to human renal autoregulation.

Flow modulates myogenic responses in isolated microperfused rabbit afferent arterioles via endothelium-derived nitric oxide.

Key Points

Structured PICO

Discussion

Implication

Cite This Study

Flow modulates myogenic responses in isolated microperfused rabbit afferent arterioles via endothelium-derived nitric oxide.

Key Points

Structured PICO

Discussion

Implication

Cite This Study

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