Vasoactive intestinal polypeptide antagonists attenuate vagally induced tachycardia in the anesthetized dog

1995 ◽  
Vol 269 (4) ◽  
pp. H1467-H1472 ◽  
Author(s):  
M. R. Hill ◽  
D. W. Wallick ◽  
L. R. Mongeon ◽  
P. J. Martin ◽  
M. N. Levy
Keyword(s):  
Vasoactive Intestinal Polypeptide ◽  
Adrenergic Receptor ◽  
Vagal Stimulation ◽  
Sinus Node ◽  
The Other ◽  
Vagus Nerves ◽  
Sinus Node Artery ◽  
Anesthetized Dogs ◽  
Intestinal Polypeptide

We used three vasoactive intestinal polypeptide (VIP) antagonists, VIP-(10-28), [p-Cl-D-Phe6,Leu17]VIP, and NT-VIP, to evaluate the role of VIP as a mediator of vagally induced tachycardia in chloralose-anesthetized dogs. After we administered muscarinic and beta-adrenergic receptor antagonists, we evoked vagally induced tachycardia either directly, by stimulating the vagus nerves for 2 min, or reflexly, by injecting phenylephrine to increase blood pressure. Furthermore, each of the antagonists attenuated the tachycardias induced by vagal stimulation by approximately 50% and the reflexly induced tachycardias by approximately 70%. Each VIP antagonist attenuated the chronotropic responses that we evoked by injecting VIP (5.2 ng/kg) into the sinus node artery. We tested the specificity of these VIP antagonists by determining whether they attenuated the increases in heart rate evoked by two other neuropeptides [peptide histidine isoleucine (PHI) and glucagon]. VIP-(10-28) attenuated the response to PHI, but not to glucagon. The other two VIP antagonists did not alter the chronotropic responses to PHI or glucagon. Our results support the hypothesis that neurally released VIP is the principal mediator of vagally induced tachycardia in the dog.

Effects of repetitive vagal stimulation on heart rate and on cardiac vasoactive intestinal polypeptide efflux

1995 ◽  
Vol 268 (5) ◽  
pp. H1939-H1946 ◽  
Author(s):  
M. R. Hill ◽  
D. W. Wallick ◽  
P. J. Martin ◽  
M. N. Levy
Keyword(s):  
Vasoactive Intestinal Polypeptide ◽  
Vagal Stimulation ◽  
Sinus Node ◽  
Cardiac Pacemaker ◽  
Close Correlation ◽  
Right Atrial ◽  
Chronotropic Response ◽  
Sinus Node Artery ◽  
Stimulation Regimen ◽  
Intestinal Polypeptide

In dogs anesthetized with alpha-chloralose, we assessed the "vagally induced tachycardia" elicited by successive 2-min periods of intense vagal stimulation (0.5 ms, 10 mA, 20 Hz) after we had blocked the animals' muscarinic and beta-adrenergic receptors with atropine and propranolol, respectively. We found that the tachycardia produced by the successive vagal stimulations progressively decreased to < 20% of the initial tachycardia response within 84 min. We also observed that the chronotropic response to vasoactive intestinal polypeptide (VIP) injected into the sinus node artery after the vagal stimulation regimen did not differ significantly from the response to the same dose of VIP injected prior to vagal stimulation. This finding indicates that the postjunctional responsiveness of the cardiac pacemaker cells had not diminished over the course of the vagal stimulation regimen. In isolated, perfused right atrial preparations, we observed a close correlation between the efflux of VIP from the atrial tissues and the chronotropic responses to vagal stimulation. Our results support the hypotheses that 1) VIP is a mediator of vagally induced tachycardia, 2) the reduction in VIP efflux is associated with a diminished vagally induced tachycardia, and 3) the reduced efflux of VIP probably reflects a diminution in neuronal release, perhaps by depletion of this peptide from the vagus nerve endings consequent to the prolonged neural stimulation.

Vasoactive intestinal polypeptide enhances automaticity of supraventricular pacemakers in anesthetized dogs

1991 ◽  
Vol 261 (2) ◽  
pp. H463-H468 ◽  
Author(s):  
D. F. Rigel ◽  
D. A. Lathrop
Keyword(s):  
Vasoactive Intestinal Polypeptide ◽  
Sinus Node ◽  
Cardiac Pacemaker ◽  
Autonomic Nerve ◽  
Beta Adrenergic ◽  
Pentobarbital Sodium ◽  
Sinus Node Artery ◽  
Anesthetized Dogs ◽  
Muscarinic Cholinergic ◽  
Intestinal Polypeptide

Effects of the cardiac neuropeptide vasoactive intestinal polypeptide (VIP) and isoproterenol (ISO) were compared on sinus nodal, subsidiary atrial, and atrioventricular junctional pacemaker automaticity in pentobarbital sodium-anesthetized dogs (n = 14). Autonomic cardiac nerves were decentralized by bilateral vagotomy and stellectomy. VIP and ISO (30, 100, and 300 pmol/kg iv) were administered during sinus rhythm and either after crushing the sinus node to unmask a latent subsidiary atrial pacemaker (n = 7 dogs) or after injecting pentobarbital sodium into the sinus node artery to elicit an atrioventricular junctional pacemaker (n = 7). Spontaneous sinus nodal, subsidiary atrial, and atrioventricular junctional pacemaker rates (after autonomic nerve decentralization) were 142 +/- 4, 114 +/- 3, and 79 +/- 4 beats/min (means +/- SE), respectively. Both VIP and ISO dose dependently increased the rates of all three pacemaker sites. Combined muscarinic-cholinergic (atropine; 0.11 mg/kg iv) and beta-adrenergic receptor blockade (nadolol; 0.5 mg/kg iv) abolished the stimulatory effects of ISO on subsidiary atrial and atrioventricular junctional pacemakers but did not affect the responses to VIP. We conclude that exogenous VIP enhances the automaticity of sinus nodal, subsidiary atrial, and atrioventricular junctional pacemakers independently of muscarinic-cholinergic and beta-adrenergic receptors. Based on the previous demonstration of VIP-immunoreactive nerves throughout the heart, our findings also suggest that endogenous VIP may be involved in cardiac pacemaker regulation.

Effects of neuropeptides on heart rate in dogs: comparison of VIP, PHI, NPY, CGRP, and NT

1988 ◽  
Vol 255 (2) ◽  
pp. H311-H317 ◽  
Author(s):  
D. F. Rigel
Keyword(s):  
Heart Rate ◽  
Neuropeptide Y ◽  
Vasoactive Intestinal Polypeptide ◽  
Sinus Node ◽  
Calcitonin Gene Related Peptide ◽  
Adrenergic Blockade ◽  
Related Peptide ◽  
Sinus Node Artery ◽  
Calcitonin Gene ◽  
Intestinal Polypeptide

This study was designed to evaluate the potential chronotropic actions of several cardiac neuropeptides in pentobarbital-anesthetized dogs. After bilateral vagotomy and stellectomy and muscarinic receptor blockade, I injected vasoactive intestinal polypeptide, peptide histidine isoleucine, neuropeptide Y, neurotensin, and calcitonin gene-related peptide into the intact sinus node artery. Neurotensin, calcitonin gene-related peptide, and neuropeptide Y exhibited no physiologically significant changes in heart rate. However, the structural homologues vasoactive intestinal polypeptide and peptide histidine isoleucine each augmented heart rate with maximal increases (approximately 120 beats/min) similar to those of norepinephrine. Vasoactive intestinal polypeptide and peptide histidine isoleucine were twice and 1/18, respectively, as potent as norepinephrine. The cardioacceleratory responses to vasoactive intestinal polypeptide and peptide histidine isoleucine were more slowly developing and longer lasting than those of norepinephrine. The responses to these two peptides were unchanged after beta-adrenergic blockade with propranolol in a dose sufficient to eliminate or greatly attenuate the norepinephrine tachycardia. These results indicate a potential role of endogenous vasoactive intestinal polypeptide and peptide histidine isoleucine in nonadrenergic, noncholinergic heart rate control in the dog.

Vasoactive intestinal polypeptide in vagally mediated pancreatic secretion of fluid and HCO3.

1979 ◽  
Vol 237 (6) ◽  
pp. E535 ◽  
Author(s):  
J Fahrenkrug ◽  
O B Schaffalitzky de Muckadell ◽  
J J Holst ◽  
S L Jensen
Keyword(s):  
Electrical Stimulation ◽  
Vasoactive Intestinal Polypeptide ◽  
Pancreatic Secretion ◽  
Vagal Stimulation ◽  
Porcine Pancreas ◽  
Pancreatic Fluid ◽  
Stimulation Of ◽  
Intestinal Polypeptide

The role of nerves that liberate vasoactive intestinal polypeptide (VIP) in the porcine pancrease as mediators of the atropine-resistant action of the vagus on flow and bicarbonate (HCO3) secretion was examined. Efferent electrical stimulation of the vagus in atropinized pigs produced a profuse flow of pancreatic juice with high HCO3 content concomitantly with a significant increase in pancreatic VIP output from 13 to 113 fmol/min. Intravenous administration of somatostatin (SRIF) during continuous electrical vagal stimulation caused a parallel suppression of the VIP release and the pancreatic fluid and HCO3 secretion to prestimulatory values. The SRIF-induced reduction in fluid and HCO3 secretion seemed to be mediated via an inhibition of the VIP release rather than through a direct effect on the exocrine cells, inasmuch as SRIF did not influence the VIP-provoked exocrine response from the in vitro isolated perfused porcine pancreas. The results support the view that VIP is transmitter in the vagally induced atropine-resistant water and HCO3 secretion from the porcine pancreas.

scholarly journals Development-Dependent Plasticity in Vasoactive Intestinal Polypeptide Neurons in the Infralimbic Cortex

2021 ◽  
Vol 2 (1) ◽  
Author(s):  
Stuart A Collins ◽  
Ipe Ninan
Keyword(s):  
Sex Differences ◽  
Anxiety Disorders ◽  
Vasoactive Intestinal Polypeptide ◽  
Cortical Plasticity ◽  
Male Mice ◽  
Infralimbic Cortex ◽  
Membrane Excitability ◽  
Gabaergic Transmission ◽  
Intestinal Polypeptide

Abstract The onset of several neuropsychiatric disorders including anxiety disorders coincides with adolescence. Consistently, threat extinction, which plays a key role in the regulation of anxiety-related behaviors, is diminished during adolescence. Furthermore, this attenuated threat extinction during adolescence is associated with an altered synaptic plasticity in the infralimbic medial prefrontal cortex (IL-mPFC), a brain region critical for threat extinction. However, the mechanism underlying the altered plasticity in the IL-mPFC during adolescence is unclear. Given the purported role of vasoactive intestinal polypeptide expressing interneurons (VIPINs) in disinhibition and hence their potential to affect cortical plasticity, we examined whether VIPINs exhibit an adolescence-specific plasticity in the IL-mPFC. We observed an increase in GABAergic transmission and a decrease in excitability in VIPINs during adolescence. Male mice show a significantly higher VIPIN-pyramidal neuron GABAergic transmission compared with female mice. The observed increase in GABAergic transmission and a decrease in membrane excitability in VIPINs during adolescence could play a role in the altered plasticity in the adolescent IL-mPFC. Furthermore, the suppression of VIPIN-mediated GABAergic transmission in females might be relevant to sex differences in anxiety disorders.

Evaluation of β-Adrenerglc Blocking Agents in Presence of Adrenergic Tone

1972 ◽  
Vol 50 (5) ◽  
pp. 381-388
Author(s):  
Victor Elharrar ◽  
Reginald A. Nadeau
Keyword(s):  
Dose Response ◽  
Sinus Node ◽  
Stellate Ganglion ◽  
Sodium Pentobarbital ◽  
Response Curves ◽  
Chronotropic Response ◽  
Blocking Agents ◽  
Sinus Node Artery ◽  
Anesthetized Dogs ◽  
The Right

The importance of the level of adrenergic tone in the determination of the dose–response curve to noradrenaline (NA) and in the evaluation of β-adrenergic blocking agents was studied in open-chest sodium pentobarbital anesthetized dogs by injecting drugs directly into the sinus node artery. Changes in the level of adrenergic tone by stimulating the right stellate ganglion resulted in variation of the observed chronotropic response to NA and of its ED50. The chronotropic responses were corrected by taking into account the underlying adrenergic tone. The negative chronotropic effect of dl-propranolol (1 and 10 μg) appeared to be related to its β-blocking properties and not to its quinidine-like effects as shown by the lack of effect of d-propranolol injected at the same doses. The magnitude of the negative chronotropic effects of 10 μg of propranolol and 100 μg of practolol, oxprenolol, and sotalol was shown to be related to the initial heart rate and consequently to the level of adrenergic tone. The comparison of these four β-blocking agents was carried out on corrected dose-response curves to NA. Their relative potencies were found to be: propranolol > oxprenolol > practolol > sotalol, corresponding to ratios of 1, [Formula: see text], [Formula: see text], and [Formula: see text]

Role of sinoatrial ring bundle in internodal conduction

1976 ◽  
Vol 231 (2) ◽  
pp. 319-325 ◽  
Author(s):  
M Hiraoka ◽  
T Sano
Keyword(s):  
Sinus Node ◽  
The Other ◽  
Wave Fronts ◽  
Av Node ◽  
Crista Terminalis ◽  
Main Route ◽  
Endocardial Surface ◽  
The Right ◽  
Activation Sequence

The role of the sinoatrial ring bundle (SARB) in internodal conduction was examined by the microelectrode technique in excised rabbit hearts. The spread of the sinus impluse to the surrounding tissues was shown to proceed anteriorly toward the right branch of the crista terminalis significantly faster than toward the other direction. Thus the right SARB and the right branch of the crista terminalis close to the sinus node were the earliest areas excited by the sinus impulse in the areas surrounding the sinus node. It was further shown that the activation sequence does not initiate from the right SARB to the right branch of the crista terminalis via the junction of these two structures. Cutting the SARB did not produce any delay in conduction from the sinus node to the atrioventricular (AV) node. The conduction velocity measured at the endocardial surface by two microelectrodes has proved that conduction in the crista terminalis was significantly faster than in the SARB. The upstroke of the action potential from the crista terminalis was also steeper than that from the SARB. These results suggest that the SARB is not the main route for impulse propagation from the sinus node to the AV node; the fastest internodal conduction therefore takes place with wide wave fronts, along the crista terminalis.

scholarly journals Chronic atropine administration diminishes the contribution of vasoactive intestinal polypeptide to heart rate regulation

2008 ◽  
pp. 827-837
Author(s):  
J Kuncová ◽  
Š Faitová ◽  
J Capouch ◽  
M Štengl ◽  
J Slavíková
Keyword(s):  
Heart Rate ◽  
Single Dose ◽  
Vasoactive Intestinal Polypeptide ◽  
Rat Heart ◽  
Vagal Stimulation ◽  
Rate Regulation ◽  
Heart Rate Regulation ◽  
The Impact ◽  
Heart Atria ◽  
Intestinal Polypeptide

Vasoactive intestinal polypeptide (VIP) is implicated in the modulation of vagal effects on the heart rate. In this study, the impact of acute and chronic atropine administration on VIP levels in rat heart atria was investigated in relation to heart rate in the course of vagus nerves stimulation. Anaesthetised control and atropinised (10 mg/kg/day for 10 days) rats pretreated with metipranolol and phentolamine that were either given or not a single dose of atropine were subjected to bilateral vagus nerve stimulation (30 min: 0.7 mA, 20 Hz, 0.2 ms). VIP concentrations in the atria were determined after each stimulation protocol. In control rats with or without single atropine administration, the heart rate upon vagal stimulation was higher than in atropinised animals with or without single atropine dose, respectively. VIP concentrations in the control atria were significantly decreased after the stimulation; the decrease was comparable both in the absence and presence of a single dose of atropine. Compared to controls, VIP levels were significantly decreased after chronic atropine treatment and they were not further reduced by vagal stimulation and single atropine administration. Administration of VIP antagonist completely abolished the differences in the heart rate upon vagal stimulation between control and atropinised groups. In conclusion, the data indicate that chronic atropine administration affects VIP synthesis in rat heart atria and consequently it modifies the heart rate regulation.

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