Overflow of catecholamine neurotransmitters to the circulation: source, fate, and functions

Esler, Murray; Jennings, Garry; Lambert, Gavin; Meredith, Ian T.; Horne, Marj; Eisenhofer, Graeme

doi:10.1152/physrev.1990.70.4.963

Cited by 737 publications

(575 citation statements)

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“…3 Along the length of terminal axons are a series of localized swellings known as "varicosities," around 1 to 3 µm and up to 4 µm in length. Most of the norepinephrine storage vesicles in a terminal axon are concentrated in these varicosities.…”

Section: Effects Of the Sympathetic Nervous System On The Normal Myocmentioning

confidence: 99%

The Role of the Autonomic Nervous System in Sudden Cardiac Death

Vaseghi

Shivkumar²

2008

Progress in Cardiovascular Diseases

317

221

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The cardiac autonomic nervous system consists of 2 branches-the sympathetic and the parasympathetic systems-that work in a delicately tuned, yet opposing fashion in the heart. This extrinsic control mechanism can dominate intrinsic regulatory mechanisms that modulate heart rate and cardiac output. These branches differ in their neurotransmitters (norepinephrine and acetylcholine) and exert stimulatory or inhibitory effects on target tissue via adrenergic and muscarinic receptors. Stimulation of the sympathetic branch exerts facilitatory effects on function, increasing heart rate and myocardial contractility, whereas the stimulation of the parasympathetic branch exerts inhibitory effects that decrease heart rate and contractility. The interplay between these two branches is complex and susceptible to control at several levels, from centrally mediated baroreceptors and chemoreceptors to local interneuronal interactions.Alterations in autonomic function occur in several interrelated cardiac conditions including sudden cardiac death, congestive heart failure, diabetic neuropathy, and myocardial ischemia. Although the full extent of these changes has not been elucidated, multiple autonomic remodeling mechanisms have been observed at both the neuronal fiber and myocardial cellular level that contribute to an arrhythmogenic substrate. We describe the anatomy of both systems in this review. However, the review will premdominantly focus on the sympathetic system, whose role in the modulation of cardiac arrhythmias is slightly better delineated. Cardiac Autonomic Innervation: NeuroanatomyBoth branches of the autonomic nervous system are composed of both afferent and efferent as well interneuronal fibers (Fig 1). Sympathetic innervation originates mainly in the right and left stellate ganglia. These fibers travel along the epicardial vascular structures of the heart and penetrate into the underlying myocardium similar to coronary vessels and end as sympathetic nerve terminals reaching the endocardium. Based on norepinephrine content studies, a gradient exists in sympathetic innervation from atria to the ventricles and from base to apex of the heart. Therefore, the atria are most densely innervated, but the ventricles are also supplied with a sympathetic network, most densely at the base. 1 Parasympathetic effects are carried by the right and left vagus nerves, originating in the medulla. The vagus nerve further divides into the superior and inferior cardiac nerves, finally merging with the postganglionic sympathetic neurons to form a plexus of nerves at the base of the heart, known as the cardiac plexus. In contrast to sympathetic neurons, after parasympathetic fibers cross the atrioventricular (AV) groove along the surface of the heart,

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Section: Effects Of the Sympathetic Nervous System On The Normal Myocmentioning

confidence: 99%

The Role of the Autonomic Nervous System in Sudden Cardiac Death

Vaseghi

Shivkumar²

2008

Progress in Cardiovascular Diseases

317

221

View full text Add to dashboard Cite

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“…Increased plasma norepinephrine may be ascribed not only to augmented sympathetic drive but also to reduced tissue clearance of norepinephrine due to altered tissue perfusion. 27 Similarly, increased heart rate does not necessarily imply increased cardiac sympathetic neural activity, given that the Neuroadrenergic influences and blood pressure variation G Grassi et al reduced inhibitory drive by the parasympathetic nervous system may also trigger a tachycardic response. 28 The microneurographic approach may show increased sympathetic neural drive in the early morning hours.…”

Section: Mechanisms Involved In Diurnal Blood Pressure Variationsmentioning

confidence: 99%

Diurnal blood pressure variation and sympathetic activity

et al. 2010

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Blood pressure changes occurring over a 24-h period are under behavioral, humoral and reflex regulation. The sympathetic nervous system modulates blood pressure variation by affecting cardiac output and peripheral vascular resistance. This paper reviews evidence for the relationship between adrenergic neural drive and blood pressure as measured by direct and indirect approaches. This paper also reviews the sympathetic activity associated with increased 'in-office' and 'out-of-office' blood pressure, that is, the white-coat and the masked-hypertensive states. Finally, this paper examines altered neuroadrenergic influences on nocturnal blood pressure reduction and blood pressure variability.

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“…The lack of a significant reduction in plasma norepinephrine levels might be explained by the fact that plasma norepinephrine levels are determined by release, metabolism, and re-uptake of neuronal released norepinephrine, possible obscuring increased release from the presynaptic neuron. 20 In summary, the present study shows that cardiac revascularization by PCI reduces central sympathetic activity in patients with clinically established myocardial ischemia, which may add beneficial effects to the increased myocardial perfusion.…”

Section: Discussionmentioning

confidence: 50%

Improving Myocardial Perfusion by Percutaneous Coronary Intervention Reduces Central Sympathetic Activity in Stable Angina

Gomes¹,

Aengevaeren²,

Lenders³

et al. 2010

Clinical Cardiology

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BackgroundBy stimulating sympathetic afferents, repetitive myocardial ischemia induces a state of increased sympathetic tone.HypothesisRemoving the ischemic trigger by revascularization using percutaneous coronary intervention (PCI) might thus reduce central sympathetic activity in symptomatically stable angina patients.MethodsA total of 20 patients with stable angina ≥ New York Heart Association (NYHA) class II with persistent symptoms despite maximal pharmacological therapy and a clinical indication for PCI, were included in our study. Sympathetic nervous system activity was measured before and 1 month after PCI by a combination of techniques: direct muscle sympathetic nerve activity (MSNA), neurochemical (plasma catecholamine levels), and heart rate variability (HRV).ResultsAll patients completed the study. After PCI there was a significant reduction in MSNA (pre‐PCI 72 ± 4 to post‐PCI 53 ± 4 burst/100 beats, P < .05) and low frequency/high frequency (LF/HF) ratio (3.7 ± 0.6 vs 2.4 ± 0.4, P < .05) consistent with a decline in sympathetic activity. Plasma norepinephrine levels were reduced after PCI, but this difference did not reach statistical significance (1.84 ± 0.17 vs 1.73 ± 0.13 nmol/L, P = not significant).ConclusionCoronary revascularization by PCI reduces sympathetic activity in patients with established myocardial ischemia. Copyright © 2010 Wiley Periodicals, Inc.

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Overflow of catecholamine neurotransmitters to the circulation: source, fate, and functions

Cited by 737 publications

References 0 publications

The Role of the Autonomic Nervous System in Sudden Cardiac Death

The Role of the Autonomic Nervous System in Sudden Cardiac Death

Diurnal blood pressure variation and sympathetic activity

Improving Myocardial Perfusion by Percutaneous Coronary Intervention Reduces Central Sympathetic Activity in Stable Angina

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