October 14, 2005The Journal of PhysiologyOpen Access

Nitric oxide blunts myogenic autoregulation in rat renal but not skeletal muscle circulation via tubuloglomerular feedback

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Population

Rat model (renal and hindlimb circulation)

Comparison

Nitric oxide synthase inhibition by l-NAME… vs Control conditions and equi-pressor dose of…

Design

Preclinical

Authors

AJArmin JustUniversity of Freiburg WAWilliam J. ArendshorstUniversity of North Carolina at Chapel Hill

Discussion

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Implication

Supports targeted NO-TGF investigation in renal disease models; hypothesis-generating and should not change clinical practice.

Structured PICO

Population

Rat model (renal and hindlimb circulation)

Intervention

Nitric oxide synthase (NOS) inhibition by l-NAME, tubuloglomerular feedback (TGF) inhibition by furosemide, and angiotensin II

Comparator

Control conditions (baseline renal arterial pressure) and equi-pressor dose of angiotensin II

Outcome

Myogenic response and balance of autoregulatory mechanisms (renal vascular resistance and autoregulation efficiency) following a 20 mmHg-step increase or decrease in renal arterial pressuresurrogate

Nitric oxide normally restrains the strength and speed of the myogenic response in renal blood flow autoregulation via a mechanism dependent on tubuloglomerular feedback.

Cite This Study

Just et al. (2005) studied this question.

synapsesocial.com/papers/6a6f99b078a11c550e09539c https://doi.org/10.1113/jphysiol.2005.094888

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Nitric oxide blunts myogenic autoregulation in rat renal but not skeletal muscle circulation via tubuloglomerular feedback

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Nitric oxide blunts myogenic autoregulation in rat renal but not skeletal muscle circulation via tubuloglomerular feedback

Discussion

Member takes

Implication

Structured PICO

Cite This Study

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Also Consider