Vasopressin secretion after stimulation of abdominal vagus in rabbit: role of A1 norepinephrine neurons

1994 ◽  
Vol 266 (6) ◽  
pp. R1885-R1890 ◽  
Author(s):  
Z. J. Gieroba ◽  
W. W. Blessing
Keyword(s):  
Electrical Stimulation ◽  
Vagus Nerve ◽  
Medulla Oblongata ◽  
Vagal Stimulation ◽  
Vagal Afferents ◽  
Neuronal Function ◽  
Plasma Vasopressin ◽  
Vasopressin Secretion ◽  
Stimulation Of

We determined whether electrical stimulation of the abdominal vagus nerve causes secretion of vasopressin in the rabbit and whether inhibition of neuronal function in the A1 region of the medulla oblongata impairs this secretion. In urethan-anesthetized rabbits, electrical stimulation of the abdominal vagus (5-min train of cathodal pulses, 0.5 ms duration, 20 Hz, 0.5-1 mA) increased plasma vasopressin from 37 +/- 8 to 133 +/- 19 pg/ml (P < 0.01, n = 11). Prior section of the cervical vagus completely prevented the increase seen with stimulation of the abdominal vagus. Injecting the inhibitory agent muscimol (1 nmol) 2 mm dorsal to the A1 area did not significantly reduce the vasopressin response to abdominal vagal stimulation. However, when muscimol was injected into the A1 area, the vagally mediated increase in plasma vasopressin was completely prevented. Our results show that stimulation of abdominal vagal afferents causes secretion of vasopressin in the rabbit via a central pathway that includes neurons in the A1 area.

Responses of medullary raphespinal neurons to electrical stimulation of thoracic sympathetic afferents, vagal afferents, and to other sensory inputs in cats

1991 ◽  
Vol 66 (6) ◽  
pp. 2084-2094 ◽  
Author(s):  
R. W. Blair ◽  
A. R. Evans
Keyword(s):  
Electrical Stimulation ◽  
Neuronal Activity ◽  
Vagal Stimulation ◽  
Discharge Rate ◽  
Stellate Ganglion ◽  
Cell Activity ◽  
Conditioning Stimulus ◽  
Vagal Afferents ◽  
Early Peak ◽  
Stimulation Of

1. Medullary raphespinal neurons antidromically activated from the T2-T5 segments were tested for responses to electrical stimulation of cervical vagal and thoracic sympathetic afferents (by stimulating the left stellate ganglion), somatic probing, auditory stimuli, and visual stimuli in cats anesthetized with alpha-chloralose. A total of 99 neurons in the raphe nuclei were studied; the locations of 76 cells were histologically confirmed. Neurons were located in raphe magnus (RM, 65%), raphe obscurus (RO, 32%), and raphe pallidus (RPa, 4%). The mean conduction velocity of these neurons was 62 +/- 2.9 (SE) m/s with a range of 1.1-121 m/s. 2. A total of 60/99 tested neurons responded to electrical stimulation of sympathetic afferents. Quantitation of responses was obtained for 55 neurons. With one exception, all responsive neurons were excited and exhibited an early burst of spikes with a mean latency of 16 +/- 1.2 ms. From a spontaneous discharge rate of 5.2 +/- 1.2 spikes/s, neuronal activity increased by 2.9 +/- 0.3 spikes/stimulus. In addition to an early peak, 15 neurons (25%) exhibited a late burst of spikes with a latency of 182 +/- 12.9 ms; neuronal activity increased by 5.0 +/- 1.3 spikes/stimulus. Duration of the late peak (130 +/- 18.5 ms) was longer than for the early peak (18 +/- 0.7 ms), but threshold voltages for eliciting each peak were comparable. Sixteen of 29 spontaneously active neurons exhibited a postexcitatory depression of activity that lasted for 163 +/- 19.1 ms. All but one tested neuron in RO responded to stimulation of sympathetic afferents, but 65% of neurons in RM responded to this stimulus. 3. In response to vagal afferent stimulation, 19% of 57 neurons exhibited inhibition only, 11% were only excited, and 9% were either excited or inhibited, depending on the stimulus paradigm used; the remaining 61% of neurons were unresponsive. From a spontaneous rate of 7.9 +/- 3.8 spikes/s, excited cells increased their discharge rate by 1.6 +/- 0.3 spikes/stimulus. Activity of inhibited cells was reduced from 21.3 +/- 5.8 to 7.8 +/- 3.1 spikes/s. The conditioning-test (CT) technique was used to assess 11 neurons' responses. Stellate ganglion stimulation was the test stimulus, and vagal stimulation the conditioning stimulus. Vagal stimulation reduced the neuronal responses to stellate ganglion stimulation by an average of 50% with a CT interval of 60-100 ms, and cell responses returned to control after 300 ms. With spontaneous cell activity, low frequencies of vagal stimulation were generally excitatory, and high frequencies (10-20 Hz) inhibitory.(ABSTRACT TRUNCATED AT 400 WORDS)

Effects of calcium channel antagonists on the vagally mediated cardiac chronotropic response in dogs

1990 ◽  
Vol 68 (10) ◽  
pp. 1363-1367 ◽  
Author(s):  
Don W. Wallick ◽  
Sherry L. Stuesse ◽  
Paul Martin
Keyword(s):  
Electrical Stimulation ◽  
Vagus Nerve ◽  
Calcium Channel ◽  
Total Dose ◽  
Cycle Length ◽  
Cardiac Cycle ◽  
Vagal Stimulation ◽  
Calcium Channel Antagonists ◽  
Chronotropic Response ◽  
Stimulation Of

A brief electrical stimulation of the vagus nerve may elicit a triphasic response comprising (i) an initial prolongation of the same or the next cardiac cycle, (ii) a return of the subsequent cardiac cycle to about the level prior to vagal stimulation, and (iii) a secondary prolongation of cardiac cycle length that lasts several beats. We compared the effects of two calcium channel antagonists, verapamil and nifedipine, on this triphasic response to vagal stimulation in chloralose-anesthetized, open-chest dogs. In the absence of vagal stimulation, nifedipine (doses of 10, 40, and 50 μg/kg for a total dose of 100 μg/kg, i.v.) and verapamil (two doses of 100 μg/kg each, i.v.) increased the cardiac cycle length (A–A interval) by 16% (429 ± 20 to 496 ± 21 ms) and 29% (470 ± 33 to 605 ± 54 ms), respectively. Nifedipine (100 μg/kg total) attenuated the initial vagally mediated prolongation of the A–A interval, from 474 ± 19 to 369 ± 42 ms above the basal A–A interval. Following the initial prolongation of the vagal effect, other A–A intervals were not affected. In contrast, verapamil potentiated the vagally mediated initial prolongation in cardiac cycle length at the first dose administered (100 μg/kg) from 492 ± 17 to 561 ± 14 ms, but other increases in dosages had no further effect. Thus these two calcium channel antagonists have different effects on the sinoatrial chronotropic responses caused by brief vagal stimulation.Key words: autonomic control, parasympathetic, heart, calcium.

EFFECTS OF VAGAL STIMULATION, VAGOTOMY AND ADRENALECTOMY ON RELEASE OF INSULIN IN THE RAT

1980 ◽  
Vol 85 (1) ◽  
pp. 131-136 ◽  
Author(s):  
TAKEO SAKAGUCHI ◽  
KEN'ICHI YAMAGUCHI
Keyword(s):  
Vagus Nerve ◽  
Plasma Insulin ◽  
Vagal Stimulation ◽  
Physiological Role ◽  
Male Rats ◽  
Pentobarbitone Sodium ◽  
Potent Factor ◽  
Adrenalectomized Rats ◽  
Stimulation Of

SUMMARY To evaluate the physiological role of the vagus nerve in the secretion of insulin in the rat, changes in plasma levels of insulin and sugar were examined after vagotomy with and without adrenalectomy. Male rats, fasted for 22 h, weighing about 300 g and anaesthetized with pentobarbitone sodium were used. Thirty minutes after unilateral or bilateral adrenalectomy, the first blood sample was taken just before pancreatic vagotomy and a second sample was taken 15 min after vagotomy. Pancreatic vagotomy significantly decreased levels of plasma insulin in bilaterally adrenalectomized rats. It was also confirmed that electrical stimulation of the pancreatic vagus nerve provoked an increase in levels of insulin associated with a reduction of carbohydrates in the blood. These observations support the theory that there is a vagal mechanism which modulates the secretion of insulin and suggest that the vagal mechanism is a potent factor although such a mechanism may be masked by the activity of the adrenal gland.

Role of the Vagus Nerve in the Antidysrhythmic Effect of Dexmedetomidine on Halothane/Epinephrine Dysrhythmias in Dogs

1995 ◽  
Vol 83 (5) ◽  
pp. 992-999 ◽  
Author(s):  
Takahiko Kamibayashi ◽  
Yukio Hayashi ◽  
Tadanori Mammoto ◽  
Atsushi Yamatodani ◽  
Koji Sumikawa ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Vagus Nerve ◽  
Neural Activity ◽  
Vagal Stimulation ◽  
Adrenergic Agonist ◽  
The Central Nervous System ◽  
Stimulation Of

Abstract Background Dexmedetomidine, an alpha2-adrenergic agonist, can prevent the genesis of halothane/epinephrine dysrhythmias through the central nervous system. Because stimulation of alpha2adrenoceptors in the central nervous system enhances vagal neural activity and vagal stimulation is known to inhibit digitalis-induced dysrhythmias, dexmedetomidine may exert the antidysrhythmic property through vagal stimulation. To address this hypothesis, the effect of dexmedetomidine in vagotomized dogs was examined and compared with that in intact dogs. In addition, the effect of vagotomy on the antidysrhythmic action of doxazosin, an alpha1antagonist, was studied.

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.

Electrical Stimulation of the Vagus Nerve Modulates the Development of Oxygen Epilepsy in Rabbits

2017 ◽  
Vol 47 (3) ◽  
pp. 345-351
Author(s):  
S. Yu. Zhilyaev ◽  
A. N. Moskvin ◽  
T. F. Platonova ◽  
I. T. Demchenko
Keyword(s):  
Electrical Stimulation ◽  
Vagus Nerve ◽  
Stimulation Of

Prolonged Apnea, Vagal Overactivity, and Sudden Infant Death

PEDIATRICS ◽  
1973 ◽  
Vol 51 (4) ◽  
pp. 755-755
Author(s):  
David S. Bachman
Keyword(s):  
At Risk ◽  
Vagus Nerve ◽  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Vagal Stimulation ◽  
Sudden Infant Death ◽  
Sudden Infant ◽  
Prolonged Apnea ◽  
Stimulation Of

The article on prolonged apnea and the sudden infant death syndrome (SIDS) by Steinschneider1 is very exciting in that it suggests the possibility of identifying infants at risk from SIDS before the final event. Obviously, it is of great importance to learn the mechanism causing the preceding apneic episodes. Do they represent vagal overactivity? Stimulation of the intact vagus nerve in the unanesthetized monkey causes apnea, as well as bradycardia and even arrhythmias.2 In fact, we have seen myocardial myocytolysis secondary to vagal stimulation.3

Sign in / Sign up

Export Citation Format

Share Document