Central neurochemical factors related to serotonin metabolism and cardiac ventricular vulnerability for repetitive electrical activity

Rabinowitz, Stephen H.; Lown, Bernard

doi:10.1016/0002-9149(78)90009-7

Cited by 41 publications

(12 citation statements)

References 33 publications

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“…These cardiovascular alterations, which are consistent with decreased efferent central sympathetic tone, are inhibited by methysergide, a serotonergic receptor antagonist (Antonaccio and Robson, 1975). Rabinowitz and Lown (1978) have demonstrated that neuropharmacological measures designed to elevate central nervous system serotonin reduced cardiac vulnerability to repetitive ventricular activity in the anesthetized dog, a result consistent with the hypothesis that elevated levels of central serotonin inhibit sympathetic neural outflow from the brain to the heart. Anton-Tay et al (1968) have shown that systemic administration of melatonin elevates serotonin levels in a region of the brain stem rich in cell bodies of serotonergic nuclei (Fig.…”

Section: Effects Of Mk-212 After Vagotomysupporting

confidence: 68%

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

Blatt¹,

Rabinowitz²,

Lown³

1979

Circulation Research

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Section: Effects Of Mk-212 After Vagotomysupporting

confidence: 68%

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

Blatt¹,

Rabinowitz²,

Lown³

1979

Circulation Research

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“…6B). Protocol 2 was repeated again by replacing calcium by manganese [21]. The addition of manganese lead to a loss of sensitivity in the CRF bio assay, and the results were therefore not useful.…”

Section: Resultsmentioning

confidence: 99%

“…7,28]. Rabinowitzand Lown [21 ] also observed a decrease in blood pressure and heart rate with 5-HTP, but an essen tially normal pressure after ¿-Tryptophan.…”

Section: Discussionmentioning

confidence: 98%

Pharmacological Evidence that Stimulation of Central Serotonergic Pathways Increases Renin Secretion

Zimmermann

Ganong²

1980

Neuroendocrinology

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To determine if serotonin plays a role in the regulation of renin secretion, pentobarbital-anesthetized dogs were injected intravenously with drugs which modify serotonin metabolism. Renal perfusion pressure was kept constant by a clamp on the aorta proximal to the renal arteries. 5-Hydroxytryptophan (5-HTP) caused a significant increase (p < 0.05) in arterial plasma renin activity (PRA) that was abolished when peripheral and central aromatic amino acid decarboxylase activities were inhibited by administration of benserazide, but not reduced when only the peripheral decarboxylase activities were inhibited by administration of carbidopa. The serotonin receptor blocking drug metergoline also abolished the renin response to 5-HTP. L-Tryptophan in two different doses increased PRA. This increase was not reduced by carbidopa but was reduced or abolished by benserazide, metergoline, and renal denervation. The increase in PRA produced by 5-HTP and L-Tryptophan occurred without any change in blood pressure. 5-HTP had no effect on heart rate but L-Tryptophan reduced heart rate. These data indicate that 5-HTP and L-Tryptophan act on the central nervous system to produce an increase in renin secretion that is mediated via the renal nerves and occurs without a concomitant increase in sympathetic output to the heart or blood vessels. The increase appears to be due to the release of serotonin within the central nervous system.

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“…In the earlier studies of Hoffman et al [2][3][4], Han et al [5], Lown et al [6], Lown and Verrier [7], Corbalan et al [8], Matta et al [1], and others [9][10][11], RET has been re garded as a pertinent index of the vulnerabil ity to VF. However, recently, reliability of RET as an index of VFT has been ques tioned by several investigators, including Jaillon et al [ 14], Obeid et al [ 16], Logic [ 13,17,18], Kowey et al [12] and Rosati et al [19].…”

Section: Relationship Between Ret and Vetmentioning

confidence: 99%

“…The repetitive extrasystole threshold (RET) has been employed as an alternative to the ventricular fibrillation threshold (VFT) in experimental studies on the vulnerability of the heart [1][2][3][4][5][6][7][8][9][10][11]. The relationship between RET and VFT observed in intact heart re mains unchanged during stellate stimulation, vagus nerve stimulation and under moderate myocardial ischemia [1,12].…”

Section: Introductionmentioning

confidence: 99%

Effects of Antiarrhythmic Drugs on the Repetitive Extrasystole Threshold and the Ventricular Fibrillation Threshold

Murakawa¹,

Toda²,

Nozaki³

et al. 1989

Cardiology

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The effects of class 1 antiarrhythmic drugs on the repetitive extrasystole threshold (RET) and the ventricular fibrillation threshold (VFT) were studied in 32 anesthetized dogs with localized transmural necrosis. All four drugs significantly increased VFT. Although lidocaine and mexiletine increased RET, procainamide and disopyramide did not. We conclude that class 1 b antiarrhythmic agents prevent ventricular fibrillation by suppressing the initiation of reentry, and that class 1 a drugs decrease the vulnerability by preventing the reentrant repetitive excitation from degenerating into chaotic multiple reentries.

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Central neurochemical factors related to serotonin metabolism and cardiac ventricular vulnerability for repetitive electrical activity

Cited by 41 publications

References 33 publications

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

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

Pharmacological Evidence that Stimulation of Central Serotonergic Pathways Increases Renin Secretion

Effects of Antiarrhythmic Drugs on the Repetitive Extrasystole Threshold and the Ventricular Fibrillation Threshold

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