Somatostatin stimulates acetylcholine release in the canine heart

Wiley, John W.; Uccioli, L.; Owyang, Chung; Yamada, Takuro

doi:10.1152/ajpheart.1989.257.2.h483

Cited by 11 publications

(15 citation statements)

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“…Although it is not well known, one of the suggested mechanisms for the octreotide-induced long QT interval is slowdown of the conducting system due to its inhibitory effects on sinoatrial and atrioventricular nodes via somatostatin receptors [16,17,18,19,20]. The recognition of a long QT interval during octreotide treatment and recovery of the interval after discontinuation led us to suggest that in our case long QT development was secondary to octreotide treatment.…”

Section: Discussionmentioning

confidence: 75%

Octreotide-Induced Long QT Syndrome in a Child with Congenital Hyperinsulinemia and a Novel Missense Mutation (p.Met115Val) in the ABCC8 Gene

Çelik¹,

Cınaz²,

Emeksiz³

et al. 2013

Horm Res Paediatr

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Background/Aims: Congenital hyperinsulinism (CHI) denotes an inappropriate secretion of insulin from pancreatic β-cells in the presence of a low blood glucose level due to various genetic causes. Diazoxide is the first-line medical treatment for CHI. In case of failure, a somatostatin analogue called octreotide is used. A prolonged QT interval is an unusual side effect of octreotide which can be lethal if unrecognized. Case Presentation: We report on a 35-day-old infant who was diagnosed with CHI on the 3rd day of his life and underwent pancreatectomy due to failure of medical treatment at 8 months. His genetic analysis revealed a compound heterozygosity for a novel missense mutation (p.Met115Val) and a nonsense mutation (p.Trp1339X) in the ABCC8 gene. Furthermore, at the 6th month of follow-up, a long QT (0.49 s) was determined by ECG examination, which was normalized following discontinuation of octreotide treatment after pancreatectomy. Thus, the long QT was considered to be secondary to octreotide medication. Conclusion: We recommend ECG monitoring before and during octreotide treatment in order to recognize a prolonged QT interval and to prevent related complications in cases with congenital hyperinsulinemia.

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Section: Discussionmentioning

confidence: 75%

Octreotide-Induced Long QT Syndrome in a Child with Congenital Hyperinsulinemia and a Novel Missense Mutation (p.Met115Val) in the ABCC8 Gene

Çelik¹,

Cınaz²,

Emeksiz³

et al. 2013

Horm Res Paediatr

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“…The actions of somatostatin, slowing the heart rate and decreasing cardiac output, closely resemble those caused by vagal stimulation. It exerts its suppressing cardiac effects by acting on calcium channels excited by b-adrenoceptor activity (Diez et al, 1985) and/or by inducing the release of acetylcholine from intracardiac parasympathetic neurons (Wiley et al, 1989), but may also modulate sympathetic neurotransmission by acting at a postjunctional site.…”

Section: Hmentioning

confidence: 99%

Autonomic innervation of the developing heart: Origins and function

2008

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Maintenance of homeostatic circulation in mammals and birds is reliant upon autonomic innervation of the heart. Neural branches of mixed cellular origin and function innervate the heart at the arterial and venous poles as it matures, eventually coupling autonomic output to the cardiac components, including the conduction system. The development of neural identity is controlled by specific networks of genes and growth factors, whereas functional properties are governed by the use of different neurotransmitters. In this review, we summarize briefly the anatomic arrangement of the vertebrate autonomic nervous system and describe, in detail, the innervation of the heart. We discuss the timing of cardiac innervation in the chick and mouse, emphasizing the relationship of the cardiac neural networks to the anatomical structures within the heart. We also discuss the variable contribution of the neural crest to vagal cardiac nerves, and summarize the main neurotransmitters secreted by the developing sympathetic and parasympathetic autonomic divisions. We provide an overview of the main growth factor and gene families involved in neural development, discussing how these factors may impact upon the development of cardiac abnormalities in congenital syndromes associated with autonomic dysfunction.

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“…This holds true for cats. Presumably, this dependence results from stimulation of acetylcholine release from parasympathetic cardiac neurons by SS [16].…”

Section: Resultsmentioning

confidence: 99%

Cardiotropic effects of somatostatin and its antagonists

et al. 1997

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Somatostatin reduces cardiac rhythm in cats, the effect being abolished by the Mcholinolytic methacin, the ganglioblocker benzohexonium, or somatostatin antagonist, Somatostatin suppresses vagal chronotropic effect by reducing its tonic component, while the synchronizing vagal component increases. The antagonist of somatostatin exerts an opposite effect: it eliminates the influence of somatostatin on the tonic vagal component and reverses its effect on the synchronizing component. Key Words: somatostatin; somatostatin antagonist; vagus; cardiac rhythmThere is considerable evidence indicating that somatostatin (SS) modulates cardiac activity. Somatostatin slows down the heart beat [10,15], elicits a negative inotropic effect [7], and decreases myocardial conductivity [6,15]. It was interesting to compare cardiotropic effects of SS with the effects of SS peptide antagonist. In the present study we examined the effects of these compounds on heart rate (HR) and parasympathetic regulation of heart rhythm in cats. MATERIALS AND METHODSExperiments were performed on 42 cats weighing 2.5-3.5 kg. The animals were anesthetized with chlomlose (75 mg/kg) and Nembutal (15 mg/qqg) and transferred to artificial ventilation. Both preparations were injected intraperitoneally. The peripheral end of the right vagus was stimulated by bursts of 3, 6, or 9 rectangular pulses (2 msec, 40 Hz) with an amplitude of 5-6 thresholds. A unipolar probe was inserted into the fight atrium via femoral vein for enhanced ECG recording. The P wave indicated the beginning of the intervalogram for SS (Sigma). The SS antagonist (7-amino-heptanoyl-Phe-D-Trp-Lys-Thr[Bzl]) was infused intravenously in 0.5 ml normal saline. The RESULTSIn the first series of experiments (n=7) we studied the effect of SS (1.3• =8 M) on HR. This peptide reduced HR from 195.6+5.2 to 180.5+4.4 beats/rain, i.e., by 7.7% (p<0.05), the latency of the effect being 23.6+3.5 sec. The maximum length of cardiac cycle was observed 45.7+4.6 sec after the onset of chronotropic reaction. Bradycardia was preserved for 6-15 rain after administration of the peptide. Repeated administrations of SS induced no tachyphylaxis. The effect of SS was abolished by pretreatment with the M-cholinolytic methacin (0.0025 mg/kg), the ganglioblocker benzohexonium (8 mg/kg), or SS antagonist (2.6x10 -8 M). The SS antagonist (n=10) had no effect on HR.In the second series of experiments we investigated the influence of SS on the dynamics of vagat chronotropic effect (VCE) induced by pulse stimulation of the vagus. In established vagal bradycardia cardiac contractions were synchronous with the rhythm of vagal stimulation. For example, with an initial HR of 194.3+4.5 beats/rain a 6-pulse stimulation of the vagus led to synchronization of vagal and cardiac rhythms which lasted from 103.5+3.4 to 84.6+4.3

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Somatostatin stimulates acetylcholine release in the canine heart

Cited by 11 publications

References 0 publications

Octreotide-Induced Long QT Syndrome in a Child with Congenital Hyperinsulinemia and a Novel Missense Mutation (p.Met115Val) in the ABCC8 Gene

Octreotide-Induced Long QT Syndrome in a Child with Congenital Hyperinsulinemia and a Novel Missense Mutation (p.Met115Val) in the ABCC8 Gene

Autonomic innervation of the developing heart: Origins and function

Cardiotropic effects of somatostatin and its antagonists

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