In vivo modulation by α2-adrenoceptors of adrenal catecholamine release in the anaesthetized dog

In this study, the reversal of the potentiating effect of idazoxan, a selective α2-antagonist, on adrenal catecholamine release elicited by splanchnic nerve stimulation in anaesthetized and vagotomized dogs, was investigated with the use of oxymetazoline, a selective α2-agonist. Stimulation of the left splanchnic nerve (5.0-V pulses of 2 ms duration for 3 min at a frequency of 2 Hz) was applied before and 20 min after the i. v. injection of each drug. Blood samples were collected in the adrenal vein before and at the end of each stimulation. The results show that the release of catecholamines induced by electrical stimulation was potentiated by 50% after idazoxan injection (0.1 mg/kg). This enhanced response was significantly antagonized by the subsequent injection of oxymetazoline (2 μg/kg). The α2-modulating effect appears to be related to the amount of catecholamines released during the stimulation, since by subgrouping of the data on the basis of the degree of potentiation by idazoxan, it was observed that this drug was more efficient when catecholamine release was higher during control stimulation. In contrast, the reversing effect of oxymetazoline was found to be more pronounced when catecholamine release was lower. These results thus suggest that the sensitivity of the α2-adrenoceptor mechanism may depend upon the in situ concentration of adrenal catecholamine release during electrical stimulation and that the potentiating effect of α2-blockade can be reversed by activation of those receptors by a selective α2-agonist.

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In vivo interactions between prejunctional α2- and β2-adrenoceptors at the level of the adrenal medulla

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y88-219 ◽

1988 ◽

Vol 66 (10) ◽

pp. 1340-1343 ◽

Cited By ~ 5

Author(s):

Sylvain Foucart ◽

Jacques de Champlain ◽

Réginald Nadeau

Keyword(s):

Electrical Stimulation ◽

Adrenal Medulla ◽

Intravenous Injection ◽

Splanchnic Nerve ◽

Inhibitory Effect ◽

Significant Rise ◽

Catecholamine Release ◽

Control Stimulation ◽

Stimulation Of

The combined effect of a β2-antagonist and an α2-agonist on the release of adrenal catecholamines was studied in the anaesthetized and vagotomized dog. The electrical stimulation of the splanchnic nerve (5-V pulses of 2 ms duration for 3 min at a frequency of 3 Hz) produced a significant rise in adrenal catecholamine release in the adrenal vein. Intravenous injection of a β2-antagonist significantly reduced this response and a subsequent injection of an α2-agonist further reduced the release of catecholamines. However, if the α2-agonist is injected first, the release is not different compared with the control stimulation, and the subsequent injection of the β2-antagonist also did not modify the release in response to electrical stimulation. These results suggest that the blockade of presynaptic β2-receptors reduces the release of adrenal catecholamines without interfering with the activation of the α2-adrenoceptors. In contrast, the pretreatment with the α2-agonist, which does not modify the release of catecholamine at 3 Hz, seems to interfere with the inhibitory effect of the β2-antagonist.

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Effects of adrenomedullin and PAMP on adrenal catecholamine release in dogs

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1999.276.4.r1118 ◽

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.

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Pancreatic and extrapancreatic galanin release during sympathetic neural activation

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1990.258.3.e436 ◽

1990 ◽

Vol 258 (3) ◽

pp. E436-E444 ◽

Cited By ~ 7

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.

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Electrical stimulation of the auditory nerve: direct current measurement in vivo

IEEE Transactions on Biomedical Engineering ◽

10.1109/10.752943 ◽

1999 ◽

Vol 46 (4) ◽

pp. 461-469 ◽

Cited By ~ 89

Author(s):

C.Q. Huang ◽

R.K. Shepherd ◽

P.M. Center ◽

P.M. Seligman ◽

B. Tabor

Keyword(s):

Electrical Stimulation ◽

Direct Current ◽

Auditory Nerve ◽

Current Measurement ◽

Direct Current Measurement ◽

Stimulation Of

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458. Extracellular levels of GABA and glutamate increase in response to direct electrical stimulation of the hippocampus in humans: an in vivo microdialysis study

Biological Psychiatry ◽

10.1016/s0006-3223(00)00728-9 ◽

2000 ◽

Vol 47 (8) ◽

pp. S140

Author(s):

W.M. Abi-Saab ◽

D.D. Spencer ◽

V. Srihari ◽

J.L. Thompson ◽

R.H. Roth ◽

...

Keyword(s):

Electrical Stimulation ◽

In Vivo Microdialysis ◽

Direct Electrical Stimulation ◽

Microdialysis Study ◽

Stimulation Of

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Hyperinsulinemia of preobese and obese fa/fa rats is partly vagus nerve mediated

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1983.244.4.e317 ◽

1983 ◽

Vol 244 (4) ◽

pp. E317-E322 ◽

Cited By ~ 7

Author(s):

F. Rohner-Jeanrenaud ◽

A. C. Hochstrasser ◽

B. Jeanrenaud

Keyword(s):

Electrical Stimulation ◽

Insulin Secretion ◽

B Cells ◽

Vagus Nerve ◽

Zucker Rats ◽

Glucose Load ◽

Parasympathetic System ◽

Enhanced Sensitivity ◽

Stimulation Of

In vivo glucose-induced insulin secretion was greater in preweaned preobese 17-day-old Zucker rats than in the corresponding controls. This hypersecretion of insulin was reversed to normal by acute pretreatment with atropine. A short-lived (30 s) electrical stimulation of the vagus nerve preceding a glucose load potentiated the in vivo glucose-induced insulin release in adult animals (6-9 wk) and more so in obese Zucker (fa/fa) than in lean rats. This suggested the existence of enhanced sensitivity and/or responsiveness of the B cells of obese animals to the parasympathetic system. That the parasympathetic tone was increased in adult obese Zucker (fa/fa) rats was corroborated by the observation that acute vagotomy of these animals resulted in a significant decrease in glucose-induced insulin secretion, whereas no such effect was seen in lean rats. Also, perfused pancreases from adult obese (fa/fa) rats oversecreted insulin during a stimulation by arginine when compared with controls, an oversecretion that was restored toward normal by superimposed infusion of atropine. It is concluded that a) the increased insulin secretion of preobese Zucker fa/fa rats is an early abnormality that is mediated by the vagus nerve, and b) increased secretion of insulin in adult obese fa/fa rats continues to be partly vagus-nerve mediated, although a decreased sympathetic tone and other unknown defects could conceivably play a role as well.

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

Biological and Pharmaceutical Bulletin ◽

10.1248/bpb.18.1207 ◽

1995 ◽

Vol 18 (9) ◽

pp. 1207-1210 ◽

Cited By ~ 4

Author(s):

Hajime KOGANEI ◽

Akihiko TAKEUCHI ◽

Tomohiko KIMURA ◽

Susumu SATOH

Keyword(s):

Nerve Stimulation ◽

Splanchnic Nerve ◽

Catecholamine Release ◽

Anesthetized Dogs ◽

Splanchnic Nerve Stimulation

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Suppression of Superficial Microglial Activation by Spinal Cord Stimulation Attenuates Neuropathic Pain Following Sciatic Nerve Injury in Rats

International Journal of Molecular Sciences ◽

10.3390/ijms21072390 ◽

2020 ◽

Vol 21 (7) ◽

pp. 2390

Author(s):

Masamichi Shinoda ◽

Satoshi Fujita ◽

Shiori Sugawara ◽

Sayaka Asano ◽

Ryo Koyama ◽

...

Keyword(s):

Spinal Cord ◽

Neuropathic Pain ◽

Electrical Stimulation ◽

Dorsal Horn ◽

Nerve Injury ◽

Spinal Cord Stimulation ◽

Microglial Activation ◽

In Vivo Optical Imaging ◽

Stimulation Of

We evaluated the mechanisms underlying the spinal cord stimulation (SCS)-induced analgesic effect on neuropathic pain following spared nerve injury (SNI). On day 3 after SNI, SCS was performed for 6 h by using electrodes paraspinally placed on the L4-S1 spinal cord. The effects of SCS and intraperitoneal minocycline administration on plantar mechanical sensitivity, microglial activation, and neuronal excitability in the L4 dorsal horn were assessed on day 3 after SNI. The somatosensory cortical responses to electrical stimulation of the hind paw on day 3 following SNI were examined by using in vivo optical imaging with a voltage-sensitive dye. On day 3 after SNI, plantar mechanical hypersensitivity and enhanced microglial activation were suppressed by minocycline or SCS, and L4 dorsal horn nociceptive neuronal hyperexcitability was suppressed by SCS. In vivo optical imaging also revealed that electrical stimulation of the hind paw-activated areas in the somatosensory cortex was decreased by SCS. The present findings suggest that SCS could suppress plantar SNI-induced neuropathic pain via inhibition of microglial activation in the L4 dorsal horn, which is involved in spinal neuronal hyperexcitability. SCS is likely to be a potential alternative and complementary medicine therapy to alleviate neuropathic pain following nerve injury.

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Dissociation between plasma, urine, and renal papillary cyclic AMP content following vasopressin and DDAVP

AJP Renal Physiology ◽

10.1152/ajprenal.1979.237.3.f218 ◽

1979 ◽

Vol 237 (3) ◽

pp. F218-F225 ◽

Cited By ~ 3

Author(s):

M. J. Bia ◽

S. Dewitt ◽

J. N. Forrest

Keyword(s):

Cyclic Amp ◽

Urine Osmolality ◽

Brattleboro Rats ◽

Renal Papilla ◽

Brattleboro Rat ◽

Clearance Studies ◽

Urinary Cyclic Amp ◽

Stimulation Of

The effects of in vivo physiologic doses of vasopressin and 1-deamino-8-D-arginine vasopressin (DDAVP) on the cyclic AMP content of plasma, urine, and renal papillary tissue were determined in the ADH-deficient Brattleboro rat. During clearance studies, plasma cyclic AMP concentrations and both total and nephrogenous urinary cyclic AMP excretion in vasopressin- and DDAVP-treated rats were similar to the values in time-matched controls. In contrast, in situ renal papillary cyclic AMP content was higher (P less than 0.001) in both vasopressin- (35.7 +/- 3.6 pmol/mg protein) and DDAVP- (29.7 +/- 2.2 pmol/mg protein) treated rats compared to controls (15.1 +/- 1.3 pmol/mg protein). Endogenous stimulation of vasopressin by dehydration in normal rats increased both papillary cyclic AMP content (27.1 +/- 2.7 pmol/mg protein) and urine osmolality, whereas no change in papillary cyclic AMP was observed following dehydration in Brattleboro rats (13.6 +/- 0.8 pmol/mg protein) despite an increase in urine osmolality. The results demonstrate that changes in cyclic AMP following in vivo vasopressin are best demonstrated by measurement of in situ cyclic AMP content of the renal papilla, whereas total urinary cyclic AMP and nephrogenous cyclic AMP are not useful indices of tubular sensitivity to this hormone.

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