scholarly journals Long-loop pathways in cardiovascular electroacupuncture responses

2009 ◽  
Vol 106 (2) ◽  
pp. 620-630 ◽  
Author(s):  
Peng Li ◽  
Stephanie C. Tjen-A-Looi ◽  
Zhi-Ling Guo ◽  
Liang-Wu Fu ◽  
John C. Longhurst
Keyword(s):  
Neuronal Activity ◽  
Nerve Stimulation ◽  
Splanchnic Nerve ◽  
Neural Recording ◽  
The Other ◽  
Ventrolateral Medulla ◽  
Neuronal Responses ◽  
Homocysteic Acid ◽  
Splanchnic Nerve Stimulation ◽  
Stimulation Of

We have shown that electroacupuncture (EA) at P 5–6 (overlying median nerves) activates arcuate (ARC) neurons, which excite the ventrolateral periaqueductal gray (vlPAG) and inhibit cardiovascular sympathoexcitatory neurons in the rostral ventrolateral medulla (rVLM). To investigate whether the ARC inhibits rVLM activity directly or indirectly, we stimulated the splanchnic nerve to activate rVLM neurons. Micropipettes were inserted in the rVLM, vlPAG, and ARC for neural recording or injection. Microinjection of kainic acid (KA; 1 mM, 50 nl) in the ARC blocked EA inhibition of the splanchnic nerve stimulation-induced reflex increases in rVLM neuronal activity. Microinjection of d,l-homocysteic acid (4 nM, 50 nl) in the ARC, like EA, inhibited reflex increases in the rVLM neuronal discharge. The vlPAG neurons receive convergent input from the ARC, splanchnic nerve, P 5–6, and other acupoints. Microinjection of KA bilaterally into the rostral vlPAG partially reversed rVLM neuronal responses and cardiovascular inhibition during d,l-homocysteic acid stimulation of the ARC. On the other hand, injection of KA into the caudal vlPAG completely reversed these responses. We also observed that ARC neurons could be antidromically activated by stimulating the rVLM, and that ARC perikarya was labeled with retrograde tracer that had been microinjected into the rVLM. These neurons frequently contained β-endorphin and c-Fos, activated by EA stimulation. Therefore, the vlPAG, particularly, the caudal vlPAG, is required for ARC inhibition of rVLM neuronal activation and subsequent EA-related cardiovascular activation. Direct projections from the ARC to the rVLM, which serve as an important source of β-endorphin, appear also to exist.

scholarly journals Pancreatic and extrapancreatic galanin release during sympathetic neural activation

1990 ◽  
Vol 258 (3) ◽  
pp. E436-E444 ◽  
Author(s):  
B. E. Dunning ◽  
P. J. Havel ◽  
R. C. Veith ◽  
G. J. Taborsky
Keyword(s):  
Electrical Stimulation ◽  
Nerve Stimulation ◽  
Splanchnic Nerve ◽  
Sympathetic Nerves ◽  
Neural Activation ◽  
Anesthetized Dogs ◽  
Basal Insulin Secretion ◽  
Peripheral Arterial ◽  
Splanchnic Nerve Stimulation ◽  
Stimulation Of

To address the hypothesis that the neutropeptide, galanin, functions as a sympathetic neurotransmitter in the endocrine pancreas, we sought to determine if galanin is released from pancreatic sympathetic nerves during their direct electrical stimulation in halothane-anesthetized dogs. During bilateral thoracic splanchnic nerve stimulation (BTSNS), both peripheral arterial and pancreatic venous levels of galanin-like immunoreactivity (GLIR) increased (delta at 10 min = +92 +/- 31 and +88 +/- 25 fmol/ml, respectively). Systemic infusions of synthetic galanin demonstrated that 1) the increment of arterial GLIR observed during BTSNS was sufficient to modestly restrain basal insulin secretion and 2) only 25% of any given increment of arterial GLIR appears in the pancreatic vein, suggesting that the pancreas extracts galanin, as it does other neurotransmitters. By use of 75% for pancreatic extraction of circulating galanin, it was calculated that pancreatic galanin spillover (output) increased by 410 +/- 110 fmol/min during BTSNS. To reinforce the conclusion that pancreatic sympathetic nerves release galanin, GLIR spillover was next measured during direct local stimulation of the pancreatic sympathetic input produced by electrical stimulation of the mixed autonomic pancreatic nerves (MPNS) in the presence of the ganglionic blocker, hexamethonium. During this local pancreatic sympathetic nerve stimulation, arterial GLIR remained unchanged, but pancreatic venous GLIR increased by 123 +/- 34 fmol/ml. Thus pancreatic GLIR spillover increased by 420 +/- 110 fmol/min during MPNS in the presence of hexamethonium. We conclude that galanin is released from both pancreatic and extrapancreatic sources during sympathetic neural activation in dogs.

Vagal and Sympathetic Innervation of the Stomach in the Skate

1935 ◽  
Vol 1 (4) ◽  
pp. 239-250 ◽  
Author(s):  
B. P. Babkin ◽  
M. H. F. Friedman ◽  
M. E. MacKay-Sawyer
Keyword(s):  
Nerve Stimulation ◽  
Intestinal Tract ◽  
Sympathetic Innervation ◽  
Splanchnic Nerve ◽  
The Other ◽  
Autonomic Nerves ◽  
Local Contraction ◽  
Small Doses ◽  
Gastro Intestinal Tract ◽  
Stimulation Of

The distribution of autonomic nerves to the gastro-intestinal tract in Raja diaphanes and R. stabuliforis is described and figured. Stimulation of the vagus or of the anterior splanchnic nerve produces movements of the stomach, much stronger for the latter nerve. Stimulation of first one nerve, then the other, results in a summation of the two effects. Stimulation (if weak) of a branch of the vagus produces local contraction only. Atropine stimulates stomach movements without interfering with the effects of nerve stimulation. Small doses of adrenaline in lateral vein produce movements in same order as after stimulation of the sympathetic (anterior splanchnic).

Excitatory projections from arcuate nucleus to ventrolateral periaqueductal gray in electroacupuncture inhibition of cardiovascular reflexes

2006 ◽  
Vol 290 (6) ◽  
pp. H2535-H2542 ◽  
Author(s):  
Peng Li ◽  
Stephanie C. Tjen-A-Looi ◽  
John C. Longhurst
Keyword(s):  
Arcuate Nucleus ◽  
Excitatory Amino Acid ◽  
Splanchnic Nerve ◽  
Periaqueductal Gray ◽  
Ventrolateral Medulla ◽  
Cardiovascular Reflexes ◽  
Inhibitory Influence ◽  
Homocysteic Acid ◽  
Electrophysiological Recordings ◽  
Stimulation Of

We have shown that the modulatory effect of electroacupuncture (EA) on the blood pressure (BP) response induced by visceral organ stimulation is related to inhibition of cardiovascular neurons in the rostral ventrolateral medulla (rVLM) through a mechanism that involves opioids. This effect is long lasting and may involve a long-loop neural supraspinal pathway, including the arcuate nucleus (ARC), which is an important site of opioid neurotransmitter synthesis. Therefore, we evaluated the role of the hypothalamic ARC and its interaction with the midbrain ventrolateral periaqueductal gray (vlPAG) in the EA-BP response. The gallbladder of α-chloralose-anesthetized cats was stimulated to test for the influence of EA on splanchnic afferent-induced cardiovascular reflexes. Electrodes were placed around the splanchnic nerve (SN), and acupuncture needles were applied at P5-6 acupoints overlying the median nerve (MN). Electrophysiological recordings showed that spontaneous activity of ARC and vlPAG neurons was low (1.3 ± 0.5 and 2.0 ± 0.5 spikes/s, respectively). We observed a gradation of responses of ARC neurons to the stimulation of different acupoints, ranging from uniform responses of all neurons during stimulation of the P5-6, LI4-11, H5-6, and St2-G2 located over deep nerves to fewer responses during stimulation of LI6-7 and G37-39 located over superficial nerves. Microinjection of the excitatory amino acid dl-homocysteic acid (DLH 4 nM, 50 nl) into the ARC augmented the responses of vlPAG neurons, whereas microinjection of kainic acid (KA 1 mM, 50 nl) to deactivate neurons in the ARC decreased vlPAG responses to SN stimulation. Thirty minutes of EA at P5-6 increased the SN-evoked discharge of vlPAG neurons (7.0 ± 1.2 to 14.3 ± 3.0 spikes/30 stimuli), a response that was blocked by microinjection of KA into the ARC. Microinjection of DLH into the ARC, like EA, inhibited (30 min) the reflex increase in BP induced by application of bradykinin (BK) to the gallbladder, whereas microinjection of KA into the ARC blocked the inhibitory influence of EA at P5-6 on the BK-induced BP response. These results suggest that excitatory projections from the ARC to the vlPAG are essential to the EA inhibition of the reflex increase in BP induced by SN or gallbladder visceral afferent stimulation.

Effects of adrenomedullin and PAMP on adrenal catecholamine release in dogs

1999 ◽  
Vol 276 (4) ◽  
pp. R1118-R1124
Author(s):  
Kimiya Masada ◽  
Takahiro Nagayama ◽  
Akio Hosokawa ◽  
Makoto Yoshida ◽  
Mizue Suzuki-Kusaba ◽  
...  
Keyword(s):  
Nerve Stimulation ◽  
Splanchnic Nerve ◽  
Catecholamine Release ◽  
Induced Response ◽  
Dependent Manner ◽  
Pentobarbital Sodium ◽  
Anesthetized Dogs ◽  
Dose Dependent ◽  
Splanchnic Nerve Stimulation

We examined the effects of proadrenomedullin-derived peptides on the release of adrenal catecholamines in response to cholinergic stimuli in pentobarbital sodium-anesthetized dogs. Drugs were administered into the adrenal gland through the phrenicoabdominal artery. Splanchnic nerve stimulation (1, 2, and 3 Hz) and ACh injection (0.75, 1.5, and 3 μg) produced frequency- or dose-dependent increases in adrenal catecholamine output. These responses were unaffected by infusion of adrenomedullin (1, 3, and 10 ng ⋅ kg−1 ⋅ min−1) or its selective antagonist adrenomedullin-(22—52) (5, 15, and 50 ng ⋅ kg−1 ⋅ min−1). Proadrenomedullin NH2-terminal 20 peptide (PAMP; 5, 15, and 50 ng ⋅ kg−1 ⋅ min−1) suppressed both the splanchnic nerve stimulation- and ACh-induced increases in catecholamine output in a dose-dependent manner. PAMP also suppressed the catecholamine release responses to the nicotinic agonist 1,1-dimethyl-4-phenylpiperazinium (0.5, 1, and 2 μg) and to muscarine (0.5, 1, and 2 μg), although the muscarine-induced response was relatively resistant to PAMP. These results suggest that PAMP, but not adrenomedullin, can act as an inhibitory regulator of adrenal catecholamine release in vivo.

Sign in / Sign up

Export Citation Format

Share Document