What is the clinical evidence from this study?

Study design: Review. Population: Cardiovascular disease. Intervention: Neuropeptide Y and galanin antagonists (proposed).

What does this research mean for the field?

Sympathetic cotransmitters such as neuropeptide Y and galanin impair cardiac vagal function and correlate with microvascular dysfunction, suggesting they may serve as therapeutic targets in cardiovascular disease. Novelty: ClaimNovelty.SYNTHESIS. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

Examine the role of peripheral postganglionic sympathetic hyperactivity and sympathetic cotransmitters in cardiovascular disease pathophysiology.

September 5, 2013AJP Regulatory Integrative and Comparative Physiology

Peripheral cardiac sympathetic hyperactivity in cardiovascular disease: role of neuropeptides

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Key result

Sympathetic cotransmitters such as neuropeptide Y and galanin impair cardiac vagal function and correlate with microvascular dysfunction, suggesting they may be therapeutic targets in cardiovascular disease.

Population

Animal models and patients with cardiovascular disease

Design

Review

Authors

JSJulia Shanks NHNeil Herring

Discussion

Member takes

Overview

May identify novel targets for vagal modulation in cardiovascular disease; leaves open prospective validation before clinical use.

Key Points

Examine the role of peripheral postganglionic sympathetic hyperactivity and sympathetic cotransmitters in cardiovascular disease pathophysiology.
Reviewed electrophysiological and neurochemical findings from spontaneously hypertensive rat models regarding stellate ganglia calcium dynamics and norepinephrine handling.
Evaluated preclinical and clinical mechanisms linking sympathetic cotransmitter release to vagal parasympathetic inhibition and coronary microvascular dysfunction during myocardial infarction.
Stellate ganglia neurons in spontaneously hypertensive models exhibit elevated calcium transients, heightened norepinephrine release, and impaired reuptake, triggering tachycardia prior to hypertension onset.
Sympathetic cotransmitters neuropeptide Y and galanin suppress vagal acetylcholine release, blunting protective parasympathetic control even during beta-adrenergic blockade.
Circulating neuropeptide Y levels correlate significantly with coronary microvascular dysfunction in patients undergoing primary percutaneous coronary intervention for ST-elevation myocardial infarction.

Structured PICO

Population

Animal models (spontaneously hypertensive rats) and patients with cardiovascular disease (myocardial infarction, chronic congestive heart failure, hypertension)

Sympathetic cotransmitters neuropeptide Y and galanin impair cardiac vagal function, suggesting that targeting their receptors could be a novel therapeutic strategy in cardiovascular diseases.

Cite This Study

Shanks et al. (2013) conducted a review in Cardiovascular disease. Neuropeptide Y and galanin antagonists (proposed) was evaluated. Sympathetic cotransmitters such as neuropeptide Y and galanin impair cardiac vagal function and correlate with microvascular dysfunction, suggesting they may be therapeutic targets in cardiovascular disease.

synapsesocial.com/papers/6a15f4bfa215942ca9e3ea8b https://doi.org/10.1152/ajpregu.00118.2013

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September 5, 2013AJP Regulatory Integrative and Comparative Physiology

Peripheral cardiac sympathetic hyperactivity in cardiovascular disease: role of neuropeptides

View Full Paper

Ask AI

Bookmark

Key result

Population

Animal models and patients with cardiovascular disease

Design

Review

Authors

JSJulia Shanks NHNeil Herring

Discussion

Member takes

Overview

May identify novel targets for vagal modulation in cardiovascular disease; leaves open prospective validation before clinical use.

Key Points

Examine the role of peripheral postganglionic sympathetic hyperactivity and sympathetic cotransmitters in cardiovascular disease pathophysiology.
Reviewed electrophysiological and neurochemical findings from spontaneously hypertensive rat models regarding stellate ganglia calcium dynamics and norepinephrine handling.
Evaluated preclinical and clinical mechanisms linking sympathetic cotransmitter release to vagal parasympathetic inhibition and coronary microvascular dysfunction during myocardial infarction.
Stellate ganglia neurons in spontaneously hypertensive models exhibit elevated calcium transients, heightened norepinephrine release, and impaired reuptake, triggering tachycardia prior to hypertension onset.
Sympathetic cotransmitters neuropeptide Y and galanin suppress vagal acetylcholine release, blunting protective parasympathetic control even during beta-adrenergic blockade.
Circulating neuropeptide Y levels correlate significantly with coronary microvascular dysfunction in patients undergoing primary percutaneous coronary intervention for ST-elevation myocardial infarction.

Structured PICO

Population

Animal models (spontaneously hypertensive rats) and patients with cardiovascular disease (myocardial infarction, chronic congestive heart failure, hypertension)

Sympathetic cotransmitters neuropeptide Y and galanin impair cardiac vagal function, suggesting that targeting their receptors could be a novel therapeutic strategy in cardiovascular diseases.

Cite This Study

synapsesocial.com/papers/6a15f4bfa215942ca9e3ea8b https://doi.org/10.1152/ajpregu.00118.2013

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