scholarly journals Neural control of biosynthesis and secretion of serum transferrin in perfused rat liver

1990 ◽  
Vol 267 (2) ◽  
pp. 545-548 ◽  
Author(s):  
Y Watanabe ◽  
A Takahashi ◽  
T Shimazu

The effects of sympathetic- and parasympathetic-nerve stimulation on the synthesis of transferrin and other serum proteins from [14C]leucine and their secretion were studied in rat liver perfused in situ. The radioactivities incorporated into perfusate transferrin, albumin and total protein increased with time during 90 min perfusion after an initial lag period of 15-30 min. The increases in the radioactivities of the perfusate proteins were inhibited by electrical stimulation of the hepatic nerve, whereas the increases were enhanced by vagal-nerve stimulation. Measurement of the incorporation of [14C]leucine into transferrin in the microsomal and cytosol fractions of the liver after 90 min perfusion revealed that the synthesis of this serum protein was suppressed by hepatic-nerve stimulation and increased by vagal-nerve stimulation. The results indicate that the biosynthesis and secretion of transferrin, and possibly other serum proteins, are inhibited by sympathetic-nerve stimulation and enhanced by parasympathetic-nerve stimulation.

1999 ◽  
Vol 276 (2) ◽  
pp. R455-R467 ◽  
Author(s):  
F. M. Smith

Convergence of inputs from extrinsic cardiac nerves [vagus and cardiopulmonary (CPN)] on intrinsic cardiac neurons was investigated in the pig ( Sus scrofa). A segment of the right atrial wall containing epicardial neurons along with attached stumps of the right vagus nerve and CPN was maintained in vitro; intracellular recordings were made from 57 neurons. Three types of neuron were identified by their responses to long intracellular depolarizing current pulses: phasic [discharged 1 action potential (AP); 40%]; accommodating (discharged multiple APs decrementing in frequency during pulse; 33%); and tonic (discharged multiple APs at a high frequency; 27%). Sixty-six percent of the neurons responded with excitatory postsynaptic potentials (EPSP) to vagal nerve stimulation; two-thirds of these cells fired APs when EPSP amplitude exceeded threshold level. Postsynaptic responses to vagal nerve stimulation were mediated by nicotinic ion channels; responses were eliminated by hexamethonium. CPN stimulation produced EPSPs but no APs in 17% of the neurons. All neurons responding with postsynaptic depolarizations to CPN stimulation also received vagal inputs. Combined stimulation of the vagus nerve and CPN produced APs in all but one of these neurons. Timolol eliminated postsynaptic responses from CPN stimulation, indicating that these responses involved β-adrenergic receptors and likely resulted from activation of sympathetic postganglionic terminals. These results show that some intrinsic cardiac neurons receive convergent inputs from the CPN and vagus nerve. It is suggested that such neurons represent intraganglionic sites for sympathetic-parasympathetic interactions in neural control of the heart.


1986 ◽  
Vol 250 (2) ◽  
pp. E212-E217 ◽  
Author(s):  
B. Ahren ◽  
T. L. Paquette ◽  
G. J. Taborsky

To investigate the effect of vagal nerve stimulation on the release of pancreatic somatostatin, we electrically stimulated (10 Hz, 5 ms, 13.5 mA, and 10 min) the thoracic vagi just below the heart in halothane anesthetized dogs (n = 15). The stimulation increased the pancreatic output of somatostatinlike immunoreactivity (SLI) (delta = +248 +/- 81 fmol/min, P less than 0.005; base-line levels = 455 +/- 150 fmol/min). min). Arterial plasma SLI levels increased as well (delta = +16 +/- 3 fmol/ml, P less than 0.001; base-line levels = 65 +/- 3 fmol/ml), reflecting stimulation of extrapancreatic SLI secretion. Significant vagal activation was verified by a fivefold increase of pancreatic output of pancreatic polypeptide (PP) (delta = +31.4 +/- 5.9 ng/min, P less than 0.001; base-line levels = 7.8 +/- 0.9 ng/min). Atropine pretreatment (n = 6) inhibited partially both the PP response (delta = +7.9 +/- 3.8 ng/min after atropine) and the pancreatic SLI response (delta = +92 +/- 29 fmol/min) to vagal nerve stimulation. However, atropine pretreatment did not modify the arterial SLI response (delta = +20 +/- 7 fmol/ml). Hexamethonium pretreatment (n = 9) completely abolished all three responses. We conclude that 1) electrical stimulation of the vagus stimulates pancreatic SLI, extrapancreatic SLI, and PP release in vivo in the dog; 2) both muscarinic and nonmuscarinic mechanisms mediate the PP and pancreatic SLI responses; 3) a nonmuscarinic mechanism mediates the extrapancreatic SLI response; and 4) all three responses are mediated via ganglionic nicotinic receptors.


Neurology ◽  
2019 ◽  
Vol 93 (5) ◽  
pp. e518-e521 ◽  
Author(s):  
Celina F. Schroeder ◽  
Maike Möller ◽  
Arne May

ObjectiveTo determine whether high placebo effects observed in recently published clinical noninvasive vagal nerve stimulation (nVNS) trials can be attributed to an active modulation of the trigeminal-autonomic reflex by the sham device.MethodsTwenty-eight healthy participants were investigated in a randomized, controlled, single-blind, within-participant design. The 4 different conditions of no stimulation, regular nVNS of the left cervical vagal nerve, stimulation of the posterior neck with the same device (sham I), and stimulation of the left cervical vagal nerve with a sham device (sham II) were applied in randomized order. Parasympathetic output (lacrimation) was provoked with kinetic oscillation stimulation (KOS) of the nasal mucosa. Lacrimation was quantified with the Schirmer II test, an objective measure of lacrimal secretion after local anesthesia, and the difference between baseline and KOS-induced lacrimation served as a measure of autonomic output.ResultsnVNS treatment resulted in a significant reduction of ipsilateral KOS-induced lacrimation compared to no stimulation (p = 0.003) and sham I (p = 0.02). A similar effect was observed for sham II (p = 0.003, p = 0.001). There was no significant difference between nVNS and sham II.ConclusionThese results suggest that both the regular nVNS and the sham device used in some of the clinical nVNS trials modulate the trigeminal-autonomic reflex. This could explain the high sham effect in these trials and suggests that stimulation of the posterior neck may be considered as a real sham condition.


2019 ◽  
Vol 11 (1) ◽  
pp. 27-36 ◽  
Author(s):  
I. G. Areshkina ◽  
D. V. Dmitrenko ◽  
N. A. Shnayder ◽  
E. A. Narodova

Stimulation of the vagal nerve is an effective treatment option in patients with pharmacoresistant epilepsy. Objective: to analyze the efficacy and safety of the Vagal Nerve Stimulation (VNS) procedure in patients suffering from pharmacoresistant epilepsy. Materials and Methods: The study included 13 patients with pharmacoresistant epilepsy, aged 5 to 38 years. Results: among these patients, 25% reported a decrease in the number of epileptic seizures within one-month time after the first session of VNS. The efficacy of the treatment improved with a prolonged use of the VNS-therapy. Despite the long duration of the current pharmacoresistant form of epilepsy in most patients, a decrease in the severity of epileptic seizures and post-seizure disorientation was noted. Side effects of VNS-therapy were recorded in 38.5% of patients; in those, a correction of VNS parameters was performed. This approach allowed us to maintain the effective VNS-therapy and correct the arising side effects. Conclusion: vagal stimulation is an effective non-pharmacological option in patients with pharmacoresistant therapy who have contraindications for surgical treatment. The VNS-therapy reduces the occurrence rate of epileptic seizures by >50% in 20-50% of patients. The VNS therapy has a good long-term efficacy in patients of any age. Stimulation of the vagal nerve is usually well tolerated.


1995 ◽  
Vol 154 (2) ◽  
pp. 213-220 ◽  
Author(s):  
K. P. KERR ◽  
F. MITCHELSON ◽  
I. M. COUPAR

2006 ◽  
Vol 37 (03) ◽  
Author(s):  
C Bussmann ◽  
HM Meinck ◽  
HH Steiner ◽  
W Broxtermann ◽  
CG Bien ◽  
...  

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