scholarly journals Effects of Yohimbine and Desipramine on Adrenal Catecholamine Release in Response to Splanchnic Nerve Stimulation in Anesthetized Dogs.

1995 ◽  
Vol 18 (9) ◽  
pp. 1207-1210 ◽  
Author(s):  
Hajime KOGANEI ◽  
Akihiko TAKEUCHI ◽  
Tomohiko KIMURA ◽  
Susumu SATOH
Keyword(s):  
Nerve Stimulation ◽  
Splanchnic Nerve ◽  
Catecholamine Release ◽  
Anesthetized Dogs ◽  
Splanchnic Nerve 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.

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.

Correlation between neural release of VIP and adrenomedullary catecholamine secretion in vivo

1995 ◽  
Vol 268 (6) ◽  
pp. R1449-R1455 ◽  
Author(s):  
R. Gaspo ◽  
N. Yamaguchi ◽  
J. de Champlain
Keyword(s):  
Adrenal Gland ◽  
Nerve Stimulation ◽  
Splanchnic Nerve ◽  
Dependent Manner ◽  
Strongly Correlated ◽  
Anesthetized Dogs ◽  
Supramaximal Stimulation ◽  
Dose Dependent ◽  
Splanchnic Nerve Stimulation

The aim of the present study was to determine whether vasoactive intestinal peptide (VIP) can be released along with catecholamines from the adrenal gland in response to direct splanchnic nerve stimulation in anesthetized dogs. An attempt was made to verify whether VIP was released mainly from chromaffin cells or from the splanchnic nerve terminals. The first group received a supramaximal stimulation (12 V) given on the left splanchnic nerve at three successive frequencies of 0.2, 2, and 20 Hz. The second group received increasing doses of 1,1-dimethyl-4-phenylpiperazinium (DMPP) locally infused into the denervated left adrenal gland. In response to nerve stimulation, adrenal venous catecholamine concentration significantly increased in a frequency-dependent manner, whereas VIP-like immunoreactive substance (VIP-ir) reached a significant level only at the highest frequency. The multiple linear regression analyses revealed that the net increases in adrenal venous catecholamine concentrations were strongly correlated with combined variables of VIP-ir concentration and frequencies, indicating r = 0.915 and 0.949 (n = 42, P < 0.0001) for epinephrine and norepinephrine concentrations, respectively. In response to local DMPP infusion, adrenal venous catecholamines increased in a dose-dependent manner, whereas VIP-ir remained unchanged. The results indicate that VIP-ir is released along with catecholamines from the dog adrenal gland in response to direct splanchnic nerve stimulation in vivo. The study also suggests that VIP is mainly released from splanchnic nerve endings.

Corelease of neuropeptide Y like immunoreactivity with catecholamines from the adrenal gland during splanchnic nerve stimulation in anesthetized dogs

1990 ◽  
Vol 68 (3) ◽  
pp. 363-369 ◽  
Author(s):  
Richard Briand ◽  
Nobuharu Yamaguchi ◽  
Jacques Gagne ◽  
Tomohiko Kimura ◽  
Lisa Farley ◽  
...  
Keyword(s):  
Adrenal Gland ◽  
Neuropeptide Y ◽  
Nerve Stimulation ◽  
Plasma Concentrations ◽  
Splanchnic Nerve ◽  
Maximum Output ◽  
Burst Stimulation ◽  
High Frequencies ◽  
Anesthetized Dogs ◽  
Splanchnic Nerve Stimulation

The release of neuropeptide Y like immunoreactivity (NPY-li) from the adrenal gland was studied in relation to the secretion of catecholamines (CA:NE, norepinephrine; E, epinephrine) during the left splanchnic nerve stimulation in thiopental–chloralose anesthetized dogs (n = 16). Plasma concentrations of NE, E, and NPY-li were determined in the left adrenal venous and aortic blood. Adrenal outputs of NPY-li, NE, and E were 2.4 ± 0.4, 1.4 ± 0.2, and 7.3 ± 1.7 ng/min, under basal conditions, respectively. These values increased significantly (p < 0.05; n = 8) in response to a continuous stepwise stimulation at frequencies of 1, 3, and 10 Hz given at 3-min intervals during 9 min, reaching a maximum output of 4.6 ± 0.9 (NPY-li), 240.2 ± 50.2 (NE), and 1412.5 ± 309.7 ng/min (E) at a frequency of 10 Hz. Burst electrical stimulation at 40 Hz for 1 s at 10-s intervals for a period of 10 min produced similar increases (p < 0.05) in the release of NPY-li (4.8 ± 1.0 ng/min, n = 8), NE (283.5 ± 144.3 ng/min, n = 8), and E (1133.5 ± 430.6 ng/min, n = 8). Adrenal NPY-li output was significantly correlated with adrenal NE output (r = 0.606; n = 24; p < 0.05) and adrenal E output (r = 0.640; n = 24; p < 0.05) in dogs receiving the burst stimulation. The present findings demonstrate that NPY-li is coreleased with NE and E from the adrenal gland in response to direct splanchnic nerve stepwise or burst stimulation at high frequencies in anesthetized dogs. It is thus possible that the adrenal medullary NPY-li contributes to the modulation of circulating NPY-li levels under various physiopathological conditions.Key words: adrenal medulla, burst stimulation, catecholamines, corelease, neuropeptide Y, splanchnic nerves.

Liver releases galanin during sympathetic nerve stimulation

1992 ◽  
Vol 262 (5) ◽  
pp. E671-E678 ◽  
Author(s):  
S. Kowalyk ◽  
R. Veith ◽  
M. Boyle ◽  
G. J. Taborsky
Keyword(s):  
Portal Vein ◽  
Femoral Artery ◽  
Nerve Stimulation ◽  
Splanchnic Nerve ◽  
Neural Activation ◽  
Sympathetic Activation ◽  
Sympathetic Nerve Stimulation ◽  
Anesthetized Dogs ◽  
A Minor ◽  
Splanchnic Nerve Stimulation

To determine whether the gut or liver releases galanin during sympathetic neural activation, we performed bilateral thoracic splanchnic nerve stimulation (BTSNS) in halothane-anesthetized dogs. Using experimentally determined galanin extraction rates of 60% for gut and no extraction by liver, calculations demonstrated a minor increase in gut spillover during BTSNS (delta = +4.8 +/- 1.8 pmol/min), whereas liver spillover of galanin-like immunoreactivity (GLIR) increased markedly (delta = +27.9 +/- 9.5 pmol/min). To confirm the finding of liver galanin release, GLIR was measured in femoral artery, portal vein, and hepatic vein during hepatic nerve stimulation (HNS). GLIR spillover from gut was not increased by HNS (delta = +1.9 +/- 6.3 pmol/min). In contrast, liver GLIR spillover was greatly increased during HNS (delta = +53.3 +/- 16.4 pmol/min). Extracts of canine liver contained 2.7 +/- 0.4 pmol GLIR/g tissue. We conclude that, despite the known significant galanin content of the gut, little galanin is released from this organ during sympathetic activation. In contrast, the liver, heretofore not described to contain galanin, contains and releases significant amounts of the peptide during sympathetic activation.

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