THE ROLE OF THE ADRENAL MEDULLA AND CORTEX IN PREVENTING INSULIN CONVULSION

1967 ◽  
Vol 17 (2) ◽  
pp. 211-219
Author(s):  
Tokuro FUKUDA
Keyword(s):  
Adrenal Medulla

Role of the Splanchnic Nerve and the Adrenal Medulla in the Genesis of ‘Preoptic Pulmonary Edema’

1956 ◽  
Vol 184 (2) ◽  
pp. 351-355 ◽  
Author(s):  
Frederick W. Maire ◽  
Harry D. Patton
Keyword(s):  
Body Weight ◽  
Protective Effect ◽  
Pulmonary Edema ◽  
Adrenal Medulla ◽  
Adrenal Glands ◽  
Splanchnic Nerve ◽  
Lung Edema ◽  
Splanchnic Nerves ◽  
Intact Rats

The pulmonary edema which follows preoptic lesions in rats is prevented by antecedent bilateral section of the splanchnic nerves. Intravenous epinephrine in doses exceeding 0.0125 mg/100 gm body weight causes fatal lung edema in rats comparable to that produced by preoptic lesions. Moreover, extracted pressor amines from rat adrenal glands cause lung edema, often fatal, when injected into the donor or into intact rats. However, adrenal demedullation does not prevent lung edema following preoptic lesions. Hence the protective effect of splanchnectomy against preoptic lesions is not wholly due to adrenal denervation. It is tentatively suggested that preoptic lung edema results from overloading of the pulmonary circuit owing to splanchnic mediated constriction of visceral venous reservoirs. Liver and spleen weights of animals dying from preoptic lung edema were significantly less than normal.

Direct effect of hypothalamic neuropeptides on the release of catecholamines by adrenal medulla in sheep – study ex vivo

2017 ◽  
Vol 20 (2) ◽  
pp. 339-346 ◽  
Author(s):  
D. Wrońska ◽  
B.F. Kania ◽  
M. Błachuta
Keyword(s):  
Adrenal Gland ◽  
Adrenal Medulla ◽  
Noradrenaline Release ◽  
Adrenocorticotropic Hormone ◽  
Ex Vivo ◽  
Adrenal System ◽  
Adrenaline Release ◽  
Hormone Control

Abstract Stress causes the activation of both the hypothalamic-pituitary-adrenocortical axis and sympatho-adrenal system, thus leading to the release from the adrenal medulla of catecholamines: adrenaline and, to a lesser degree, noradrenaline. It has been established that in addition to catecholamines, the adrenomedullary cells produce a variety of neuropeptides, including corticoliberine (CRH), vasopressin (AVP), oxytocin (OXY) and proopiomelanocortine (POMC) – a precursor of the adrenocorticotropic hormone (ACTH). The aim of this study was to investigate adrenal medulla activity in vitro depending, on a dose of CRH, AVP and OXY on adrenaline and noradrenaline release. Pieces of sheep adrenal medulla tissue (about 50 mg) were put on 24-well plates and were incubated in 1 mL of Eagle medium without hormone (control) or supplemented only once with CRH, AVP and OXY in three doses (10−7, 10−8 and 10−9 M) in a volume of 10 μL. The results showed that CRH stimulates adrenaline and noradrenaline release from the adrenal medulla tissue. The stimulating influence of AVP on adrenaline release was visible after the application of the two lower doses of this neuropeptide; however, AVP reduced noradrenaline release from the adrenal medulla tissue. A strong, inhibitory OXY effect on catecholamine release was observed, regardless of the dose of this hormone. Our results indicate the important role of OXY in the inhibition of adrenal gland activity and thus a better adaptation to stress on the adrenal gland level.

scholarly journals RNA-seq of Isolated Chromaffin Cells Highlights the Role of Sex-Linked and Imprinted Genes in Adrenal Medulla Development

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Wing Hei Chan ◽  
Masayuki Komada ◽  
Toshiaki Fukushima ◽  
E. Michelle Southard-Smith ◽  
Colin R. Anderson ◽  
...  
Keyword(s):  
Adrenal Medulla ◽  
Chromaffin Cells ◽  
Imprinted Genes ◽  
Rna Seq

Pressor response to chemoreflex activation in awake rats: role of vasopressin and adrenal medulla

2005 ◽  
Vol 84 (1) ◽  
pp. 39-44 ◽  
Author(s):  
Luciano G. Fernandes ◽  
Vagner R. Antunes ◽  
Leni G.H. Bonagamba ◽  
Benedito H. Machado
Keyword(s):  
Adrenal Medulla ◽  
Pressor Response ◽  
Awake Rats

scholarly journals Inositol 1,3,4,5-tetrakisphosphate-induced Ca2+ sequestration into bovine adrenal-medullary secretory vesicles

1991 ◽  
Vol 278 (2) ◽  
pp. 381-385 ◽  
Author(s):  
S H Yoo
Keyword(s):  
Adrenal Medulla ◽  
Exchange Mechanism ◽  
Secretory Vesicles ◽  
Bovine Adrenal Medulla ◽  
Ca2 Channels

Ins(1,3,4,5)P4 induced a rapid sequestration of Ca2+ into both secretory vesicles and microsomes of bovine adrenal medulla. The Ca(2+)-sequestering role of Ins(1,3,4,5)P4 contrasts with the Ca(2+)-releasing role of Ins(1,4,5)P3 in adrenal-medullary secretory vesicles and microsomes. The Ins(1,3,4,5)P4-induced Ca2+ sequestration into secretory vesicles was not inhibited by heparin (50 micrograms/ml), whereas Ins(1,4,5)P3-induced Ca2+ release was completely inhibited, indicating two different receptors for Ins(1,4,5)P3 and Ins(1,3,4,5)P4. Furthermore, Ins(1,3,4,5)P4 was as effective at 4 degrees C as at 24 degrees C in sequestering Ca2+ into secretory vesicles, implying Ca2+ sequestration through receptor-operated Ca2+ channels or activation of the Ca(2+)-exchange mechanism by Ins(1,3,4,5)P4. The Ca(2+)-sequestering activity of Ins(1,3,4,5)P4 has also been demonstrated with 45Ca2+; 10 microM-Ins(1,3,4,5)P4 induced rapid uptake of 45Ca2+ into secretory vesicles optimized for Ca2+ uptake, whereas 10 microM-Ins(1,4,5)P3 induced 45Ca2+ release from secretory vesicles in similar experiments.

scholarly journals Blockade of Adrenal Medulla-Derived Epinephrine Potentiates Bee Venom-Induced Antinociception in the Mouse Formalin Test: Involvement of Peripheralβ-Adrenoceptors

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Suk-Yun Kang ◽  
Dae-Hyun Roh ◽  
Hyun-Woo Kim ◽  
Ho-Jae Han ◽  
Alvin J. Beitz ◽  
...  
Keyword(s):  
Adrenal Medulla ◽  
Formalin Test ◽  
Late Phase ◽  
Antinociceptive Effect ◽  
Bee Venom ◽  
Pain Models ◽  
Adrenergic Antagonists ◽  
Novel Strategy ◽  
Chronic Pain Conditions

The injection of diluted bee venom (DBV) into an acupoint has been used traditionally in eastern medicine to treat a variety of inflammatory chronic pain conditions. We have previously shown that DBV had a potent antinociceptive efficacy in several rodent pain models. However, the peripheral mechanisms underlying DBV-induced antinociception remain unclear. The present study was designed to investigate the role of peripheral epinephrine on the DBV-induced antinociceptive effect in the mouse formalin assay. Adrenalectomy significantly enhanced the antinociceptive effect of DBV during the late phase of the formalin test, while chemical sympathectomy had no effect. Intraperitoneal injection of epinephrine blocked this adrenalectomy-induced enhancement of the DBV-induced antinociceptive effect. Moreover, injection of a phenylethanolamine N-methyltransferase (PNMT) inhibitor enhanced the DBV-induced antinociceptive effect. Administration of nonselectiveβ-adrenergic antagonists also significantly potentiated this DBV-induced antinociception, in a manner similar to adrenalectomy. These results demonstrate that the antinociceptive effect of DBV treatment can be significantly enhanced by modulation of adrenal medulla-derived epinephrine and this effect is mediated by peripheralβ-adrenoceptors. Thus, DBV acupoint stimulation in combination with inhibition of peripheralβ-adrenoceptors could be a potentially novel strategy for the management of inflammatory pain.

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