What question did this study set out to answer?

To determine whether enhanced tubuloglomerular feedback in spontaneously hypertensive rats is caused by oxygen radical-mediated inactivation of nitric oxide.

May 1, 2000AJP Renal Physiology

Roles of NO and oxygen radicals in tubuloglomerular feedback in SHR

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Population

Spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY)

Comparison

Microperfusion of tempol (10 M), 7-nitroindazole… vs Wistar-Kyoto rats (WKY) and baseline responses

Design

Preclinical

Authors

WWWilliam J. WelchUniversity of New Brunswick ATAkihiro TojoDokkyo Medical University CWChristopher S. WilcoxVascular Medicine

Discussion

Member takes

Implication

Supports oxidative stress impairing NO-TGF regulation in SHR; hypothesis-generating and should not yet change clinical practice.

Key Points

To determine whether enhanced tubuloglomerular feedback in spontaneously hypertensive rats is caused by oxygen radical-mediated inactivation of nitric oxide.
Assessed tubuloglomerular feedback (TGF) via proximal stop-flow pressure (PSF) measurements during loop of Henle (LH) microperfusion with artificial tubular fluid in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) controls.
Administered the nNOS inhibitor 7-nitroindazole (7-NI, 10⁻⁴ M), the NO donor SNAP (10⁻⁷–10⁻⁴ M), and the superoxide dismutase mimetic tempol (10⁻⁴ M) via peritubular capillary and LH microperfusion.
Maximum TGF responses were significantly higher in SHR (10.8 ± 0.4 mm Hg, n=39 nephrons) than in WKY rats (8.8 ± 0.4 mm Hg, n=30 nephrons, P < 0.001), accompanied by increased renal cortical nitrotyrosine expression (P < 0.05).
TGF in SHR was unresponsive to nNOS inhibition with 7-NI (10.0 ± 0.7 to 10.5 ± 0.8 mm Hg, n=8, not significant) compared to WKY (8.3 ± 0.3 to 10.8 ± 0.4 mm Hg, n=8, P < 0.001), and showed blunted sensitivity to the NO donor SNAP (P < 0.05).
Peritubular capillary perfusion of tempol blunted TGF significantly more in SHR (32 ± 3%, n=10) than in WKY (19 ± 6%, n=10, P < 0.05) and normalized TGF responsiveness to 7-NI and SNAP in SHR nephrons.

Structured PICO

Population

Spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY)

Intervention

Microperfusion of tempol (10(-4) M), 7-nitroindazole (7-NI, 10(-4) M), and S-nitroso-N-acetyl-penicillamine (SNAP, 10(-7)-10(-4) M)

Comparator

Wistar-Kyoto rats (WKY) and baseline responses

Outcome

Maximum tubuloglomerular feedback (TGF) responses, assessed from changes in proximal stop-flow pressure (P(SF))surrogate

In spontaneously hypertensive rats, enhanced tubuloglomerular feedback responses are partly due to oxygen radicals inactivating locally generated nitric oxide.

Cite This Study

Welch et al. (2000) studied this question.

synapsesocial.com/papers/6a71368bf44fa9f079defd92 https://doi.org/10.1152/ajprenal.2000.278.5.f769

Topics

Hypertension management

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Roles of NO and oxygen radicals in tubuloglomerular feedback in SHR

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Topics

Roles of NO and oxygen radicals in tubuloglomerular feedback in SHR

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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