What question did this study set out to answer?

To identify the intracellular signal transduction pathway responsible for angiotensin II type 2 receptor-mediated stimulation of delayed rectifier potassium currents in brain neurons.

November 1, 1994AJP Cell Physiology

Angiotensin II type 2 receptor stimulation of neuronal K+ currents involves an inhibitory GTP binding protein

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Population

Neurons cocultured from rat hypothalamus and brain stem

Design

Preclinical

Authors

JKJian KangGansu Provincial Hospital PPPhilip PosnerFlorida State University CSColin SumnersPreventive Cardiology

Discussion

Member takes

Overview

Should not alter clinical management; leaves open whether Gi-PP2A signaling translates to human neuronal AT2 effects.

Key Points

To identify the intracellular signal transduction pathway responsible for angiotensin II type 2 receptor-mediated stimulation of delayed rectifier potassium currents in brain neurons.
Cultured rat hypothalamic and brain stem neurons were treated with 100 nM angiotensin II to elicit delayed rectifier K+ currents.
Signaling pathways were probed using pertussis toxin (200 ng/ml), intracellular antibodies against G-protein alpha subunits (anti-Gi, anti-Go, anti-Gq/11), and phosphatase inhibitors including okadaic acid, anti-PP2A antibodies, and sodium orthovanadate.
Angiotensin II-induced stimulation of potassium currents was abolished by pertussis toxin pretreatment and intracellular anti-Gi alpha antibodies, while anti-Go alpha and anti-Gq/11 alpha antibodies had no effect.
The potassium current stimulation was inhibited by okadaic acid (1-10 nM) and anti-PP2A antibodies, but was unaffected by sodium orthovanadate (1 mM).

Structured PICO

Population

Neurons cocultured from rat hypothalamus and brain stem

Intervention

Angiotensin II (100 nM) with or without pertussis toxin (200 ng/ml), anti-Gi alpha antibody (1:200), okadaic acid (1-10 nM), or anti-PP2A antibodies

Outcome

Outward K+ current (IK; delayed rectifier K+ current)

Gi and PP2A are identified as key components of the signal transduction pathway responsible for AT2-receptor-mediated stimulation of neuronal K+ currents.

Cite This Study

Kang et al. (1994) studied this question.

synapsesocial.com/papers/6a701eda31a3df824328660e https://doi.org/10.1152/ajpcell.1994.267.5.c1389

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November 1, 1994AJP Cell Physiology

Angiotensin II type 2 receptor stimulation of neuronal K+ currents involves an inhibitory GTP binding protein

View Full Paper

Ask AI

Bookmark

Population

Neurons cocultured from rat hypothalamus and brain stem

Design

Preclinical

Authors

JKJian KangGansu Provincial Hospital PPPhilip PosnerFlorida State University CSColin SumnersPreventive Cardiology

Discussion

Member takes

Overview

Should not alter clinical management; leaves open whether Gi-PP2A signaling translates to human neuronal AT2 effects.

Key Points

To identify the intracellular signal transduction pathway responsible for angiotensin II type 2 receptor-mediated stimulation of delayed rectifier potassium currents in brain neurons.
Cultured rat hypothalamic and brain stem neurons were treated with 100 nM angiotensin II to elicit delayed rectifier K+ currents.
Signaling pathways were probed using pertussis toxin (200 ng/ml), intracellular antibodies against G-protein alpha subunits (anti-Gi, anti-Go, anti-Gq/11), and phosphatase inhibitors including okadaic acid, anti-PP2A antibodies, and sodium orthovanadate.
Angiotensin II-induced stimulation of potassium currents was abolished by pertussis toxin pretreatment and intracellular anti-Gi alpha antibodies, while anti-Go alpha and anti-Gq/11 alpha antibodies had no effect.
The potassium current stimulation was inhibited by okadaic acid (1-10 nM) and anti-PP2A antibodies, but was unaffected by sodium orthovanadate (1 mM).

Structured PICO

Population

Neurons cocultured from rat hypothalamus and brain stem

Intervention

Angiotensin II (100 nM) with or without pertussis toxin (200 ng/ml), anti-Gi alpha antibody (1:200), okadaic acid (1-10 nM), or anti-PP2A antibodies

Outcome

Outward K+ current (IK; delayed rectifier K+ current)

Gi and PP2A are identified as key components of the signal transduction pathway responsible for AT2-receptor-mediated stimulation of neuronal K+ currents.

Cite This Study

Kang et al. (1994) studied this question.

synapsesocial.com/papers/6a701eda31a3df824328660e https://doi.org/10.1152/ajpcell.1994.267.5.c1389

Also Consider

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