What question did this study set out to answer?

To determine whether phosphodiesterase 2A activity limits the ability of B-type natriuretic peptide to suppress sympathetic neurotransmission via cyclic guanosine monophosphate pathways.

April 28, 2015Hypertension

Efficacy of B-Type Natriuretic Peptide Is Coupled to Phosphodiesterase 2A in Cardiac Sympathetic Neurons

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Population

In vitro atrial preparations, isolated cardiac sympathetic neurons, and stellate neurons from…

Comparison

B-type natriuretic peptide application and… vs Baseline conditions, normotensive controls, and…

Design

Preclinical

Authors

DLDan LiGeneral Cardiology CLChieh‐Ju LuCentre for Human Genetics GHGuoliang HaoHenan Academy of Sciences

Discussion

Member takes

Implication

PDE2A may blunt BNP sympathoinhibition in hypertension; hypothesis-generating and leaves open translation to human disease.

Key Points

To determine whether phosphodiesterase 2A activity limits the ability of B-type natriuretic peptide to suppress sympathetic neurotransmission via cyclic guanosine monophosphate pathways.
Measured norepinephrine release and heart rate changes following sympathetic nerve stimulation in isolated atrial preparations and sympathetic neurons.
Assessed calcium currents, intracellular calcium transients, and cyclic nucleotide levels using electrophysiological recording, fluorescence imaging, and FRET assays.
Overexpressed phosphodiesterase 2A via adenoviral gene transfer and compared baseline phosphodiesterase 2A activity in stellate neurons from prohypertensive versus normotensive rats.
B-type natriuretic peptide decreased norepinephrine release, heart rate responses, and depolarization-evoked calcium transients through a cyclic guanosine monophosphate and protein kinase G pathway without altering cyclic adenosine monophosphate.
Adenoviral overexpression of phosphodiesterase 2A eliminated B-type natriuretic peptide-induced cyclic guanosine monophosphate elevation and prevented reductions in calcium currents, calcium transients, and neurotransmitter release, which was rescued by phosphodiesterase 2A inhibition.
Phosphodiesterase 2A activity was significantly elevated in stellate neurons from prohypertensive rats relative to normotensive control animals.

Structured PICO

Population

In vitro atrial preparations, isolated cardiac sympathetic neurons, and stellate neurons from prohypertensive rats and normotensive controls

Intervention

B-type natriuretic peptide (BNP) application and phosphodiesterase 2A (PDE2A) overexpression via adenoviral gene transfer

Comparator

Baseline conditions, normotensive controls, and PDE2A inhibition

Outcome

Norepinephrine release, heart rate responses to sympathetic nerve stimulation, and intracellular calcium transientssurrogate

Abnormally high levels of phosphodiesterase 2A may blunt the inhibitory action of BNP on sympathetic transmission, potentially explaining paradoxical proadrenergic actions in cardiovascular disease.

Cite This Study

Li et al. (2015) studied this question.

synapsesocial.com/papers/6a834457d4f0d3e447933971 https://doi.org/10.1161/hypertensionaha.114.05054

Topics

Hypertension management

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Efficacy of B-Type Natriuretic Peptide Is Coupled to Phosphodiesterase 2A in Cardiac Sympathetic Neurons

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Topics

Efficacy of B-Type Natriuretic Peptide Is Coupled to Phosphodiesterase 2A in Cardiac Sympathetic Neurons

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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