Central serotonergic agents raise the repetitive extrasystole threshold of the vulnerable period of the canine ventricular myocardium.

Blatt, Charles M.; Rabinowitz, Stephen H.; Lown, Bernard

doi:10.1161/01.res.44.5.723

Cited by 33 publications

(14 citation statements)

References 32 publications

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“…if arrhythmias are to be controlled and prevented by interventions aimed at modifying neural cardiac traffic, blunting the genesis at their source within the brain is an attractive challenge.'' (Blatt et al, 1979). We believe that our recent findings form a solid evidence for the idea of using 5-HT1A agonists as central sympatholytic cardioprotective drugs.…”

Section: Clinical Perspectives Of New Applications For 5-ht1a Agonistsmentioning

confidence: 52%

Central 5-HT receptors in cardiovascular control during stress

Nalivaiko

Sgoifo

2009

Neuroscience & Biobehavioral Reviews

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Section: Clinical Perspectives Of New Applications For 5-ht1a Agonistsmentioning

confidence: 52%

Central 5-HT receptors in cardiovascular control during stress

Nalivaiko

Sgoifo

2009

Neuroscience & Biobehavioral Reviews

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“…"-" If dogs were pretreated with a selective extracerebral decarboxylase inhibitor (25 mg/kg MK-486), 5-HTP still produced a depressor response, but instead of increasing HR, bradycardia was seen; however, inhibition of both cerebral and extracerebral decarboxylase (25 mg/kg i.v., Ro4-4602) prevented the 5-HTP effect on both BP and BCO. 86 -** In contrast to these studies, Dunkley et al 8 7 observed that 30 mg/kg 5-HTP i.v. in conscious dogs produced a pressor effect of approximately 20-50 mm Hg 30 minutes after injection.…”

Section: -Hydroxytryptophanmentioning

confidence: 94%

Review of the role of the central serotonergic neuronal system in blood pressure regulation.

1980

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SUMMARY Alterations in the dynamics of brain serotonin biosynthesis can lead to changes in cardiovascular function. It appears that the activation of cerebral serotonin receptors produces a pressor effect in normotensive rats but produces a depressor effect in nonnotensive cats or dogs. On the other hand, reductions in the levels of serotonin can prevent the onset of hypertension in some experimental hypertensive models and lower the blood pressure of organisms with established hypertension. The ability of brain serotonin to modulate arterial blood pressure may be mediated by the influences of the serotonergic neuronal systems on efferent sympathetic activity. Finally, the reduction in sympathetic outflow produced by increasing brain serotonin levels in dogs protects the heart against ventricular fibrillation and may, therefore, constitute a reasonable adjunct in the management of high-risk, cardiac-arrest patients. (Hypertension 2: 243-255, 1980) KEYWORDS * serotonin • blood pressure • sympathetic outflow I T seems somewhat paradoxical that so little is known about the cardiovascular function of a substance first referred to by physiologists as vasotonin or thrombotonin (i.e., serotonin). It was not until the chemical structure of serotonin was actually identified as 5-hydroxytryptamine (5-HT) 1 that progress was made in the understanding of the peripheral effects of 5-HT on the cardiovascular system. Unfortunately, much less progress has been made in identifying the central (brain) effects of 5-HT on blood pressure and heart rate. A precedent for studying the central role of 5-HT on heart function was first set by early studies on the cardiovascular pharmacology of intracerebrally injected 5-HT and its precursors; 2 however, it was perhaps the pioneering work of Dahlstrom and Fuxe, s demonstrating the existence of discrete 5-HT-containing neurons in the brain, and the apparent "coincidence" of these medullary indolamine tracts with previously identified neural pathways controlling cardiovascular regulation 4 -6 that provided the greatest impetus to the study of this neurotransmitter system in regulating blood pressure. Moreover, since the ramifications of the 5-

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“…Using repetitive extrasystole threshold as an index of ventricular vulnerability, Lown et al. demonstrated in several follow‐up studies the cardioprotective properties of systemically administered serotonin (5‐hydroxytryptamine; 5‐HT) precursors, agonists or agents affecting central 5‐HT levels 27,28 . These cardioprotective effects were associated with an increase in 5‐HT content in the cerebrospinal fluid and were largely mediated by reduced cardiac sympathetic nerve activity, unequivocally confirming that the effects were central 29 .…”

Section: Cardiac Disturbances Provoked By Acute Psychological Stressesmentioning

confidence: 97%

Animal models of psychogenic cardiovascular disorders: what we can learn from them and what we cannot

Nalivaiko

2011

Clin Exp Pharma Physio

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1. Epidemiological and clinical studies from the past 50 years provide unequivocal evidence for a close association and causative links between psychological stresses and cardiovascular dysfunction in humans. Not surprisingly, numerous animal experiments have been undertaken in an attempt to clarify underlying pathophysiological mechanisms. The present review focuses on animal models that provide insight into the mechanisms of stress-induced cardiovascular dysfunction. 2. Great success was achieved in elucidating the neural pathways and neurotransmitters responsible for the cardiac consequences of acute stressors, such as stress-induced ventricular arrhythmias and stress cardiomyopathy. These disturbances were reproduced successfully in canine and rodent models. The most important finding from these animal models is that these disturbances are mediated by elevated sympathetic outflow to the ventricular myocardium. 3. In contrast, attempts to induce psychogenic hypertension in rodents produced inconsistent and contentious results. More recent studies using biotelemetry raised serious doubts regarding the validity of earlier results obtained with the tail-cuff method and it remains unclear whether chronic stress can lead to sustained hypertension in animal models.

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Central serotonergic agents raise the repetitive extrasystole threshold of the vulnerable period of the canine ventricular myocardium.

Cited by 33 publications

References 32 publications

Central 5-HT receptors in cardiovascular control during stress

Central 5-HT receptors in cardiovascular control during stress

Review of the role of the central serotonergic neuronal system in blood pressure regulation.

Animal models of psychogenic cardiovascular disorders: what we can learn from them and what we cannot

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