What question did this study set out to answer?

To examine how diverse bioactive angiotensin metabolites influence renal vascular resistance and renal nerve stimulation-evoked noradrenaline release in isolated rat kidneys.

June 27, 2003Journal of Hypertension

Effects of angiotensin-(1-7) and other bioactive components of the renin–angiotensin system on vascular resistance and noradrenaline release in rat kidney

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Population

Rat isolated kidney model

Design

Preclinical

Authors

JSJohannes StegbauerDüsseldorf University Hospital OVOliver VonendDeutsche Post (Germany)VOVitus OberhauserUniversity of Freiburg

Discussion

Member takes

Implication

Animal data extend RAS peptide insights; human relevance and therapeutic translation remain untested.

Key Points

To examine how diverse bioactive angiotensin metabolites influence renal vascular resistance and renal nerve stimulation-evoked noradrenaline release in isolated rat kidneys.
Perfused isolated rat kidneys with Ang I, Ang II, Ang III, Ang IV, des-Asp-Ang I, and Ang-(1-7) under electrical renal nerve stimulation.
Tested regulatory mechanisms using the AT1 antagonist EXP 3174 (0.1 µmol/l), AT2 antagonist PD 123319 (1 µmol/l), ACE inhibitor captopril (10 µmol/l), and Ang-(1-7) antagonist d-Ala7-Ang-(1-7) (10 µmol/l).
Ang I, Ang II, Ang III, Ang IV, and des-Asp-Ang I produced concentration-dependent pressor responses and increased noradrenaline release, with potency ranking Ang II ≥ Ang III > Ang I = des-Asp-Ang I > Ang IV.
All vascular and neurotransmitter responses were blocked by the AT1 antagonist EXP 3174, whereas captopril selectively eliminated the effects of Ang I and des-Asp-Ang I.
Ang-(1-7) showed no intrinsic vasoactive or neuromodulatory action but blocked the effects of Ang I and Ang II, demonstrating 10-fold greater potency against Ang I.

Structured PICO

Population

Rat isolated kidney model

Intervention

Angiotensin metabolites (Ang I, Ang II, Ang III, Ang IV, des-Asp-Ang I, Ang-(1-7)) and various antagonists (EXP 3174, PD 123319, captopril, d-Ala7-Ang-(1-7))

Outcome

Vascular resistance and noradrenaline release to renal nerve stimulation (RNS)surrogate

Angiotensin metabolites regulate renal vascular resistance and noradrenaline release via AT1 receptors, with Ang-(1-7) acting as a potent endogenous inhibitor.

Cite This Study

Stegbauer et al. (2003) studied this question.

synapsesocial.com/papers/6a7dc6270380f7c7805ca0ac https://doi.org/10.1097/00004872-200307000-00030

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Effects of angiotensin-(1-7) and other bioactive components of the renin–angiotensin system on vascular resistance and noradrenaline release in rat kidney

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Effects of angiotensin-(1-7) and other bioactive components of the renin–angiotensin system on vascular resistance and noradrenaline release in rat kidney

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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