scholarly journals Central sympathetic nerve activation in subarachnoid hemorrhage

2021 ◽  
Author(s):  
Yu Hasegawa ◽  
Hiroki Uchikawa ◽  
Sosho Kajiwara ◽  
Motohiro Morioka
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activation

The effect of vasodilatation and sympathetic nerve activation on net water absorption in the cat's small intestine

1979 ◽  
Vol 106 (1) ◽  
pp. 61-68 ◽  
Author(s):  
INGEMAR BRUNSSON ◽  
STEFAN EKLUND ◽  
MATS JODAL ◽  
OVE LUNDGREN ◽  
HENRIK SJÖVALL
Keyword(s):  
Small Intestine ◽  
Water Absorption ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activation

scholarly journals Differential Renal and Lumbar Sympathetic Nerve Activation Following Myocardial Infarction in Rats

2019 ◽  
Vol 33 (S1) ◽  
Author(s):  
Misa Yoshimoto ◽  
Shizuka Ikegame ◽  
Fumi Hyodo ◽  
Yuki Shiwa ◽  
Kenju Miki
Keyword(s):  
Myocardial Infarction ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activation

Abstract 221: Sympathetic and Metabolic Consequences of Deleting the Insulin Receptor from Proopiomelanocortin Neurons

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Kenjiro Muta ◽  
Donald A Morgan ◽  
Balyssa B Bell ◽  
Kamal Rahmouni
Keyword(s):  
Insulin Receptor ◽  
Sympathetic Nerve ◽  
Energy Homeostasis ◽  
Neuronal Population ◽  
Brown Adipose ◽  
Significant Difference ◽  
Insulin Receptor Signaling ◽  
Hypothalamic Arcuate Nucleus ◽  
Cre Recombination ◽  
Sympathetic Nerve Activation

Hypothalamic insulin receptor (IR) signaling has been implicated in the regulation of energy homeostasis and sympathetic nerve activity (SNA). Recent studies demonstrated that the sympathetic action of insulin emanates from the hypothalamic arcuate nucleus (ARC). However, the specific neuronal population within the ARC that mediates the sympathetic effect of insulin is unknown. We hypothesized that proopiomelanocortin (POMC) neurons of the ARC which contain the insulin receptor (IR) are critical for the increases in SNA in response to insulin. To test this, we generated mice lacking the IR specifically in POMC neurons (IRΔPOMC mice) by crossing the IRflox/flox mice with POMCCre mice. First, we visualized POMC promoter-driven Cre recombinase expression by crossing POMCCre mice with tdTomato reporter mice. tdTomato fluorescence was detected mainly in the ARC and overlapped with staining for β-endorphin (a POMC proteolytic product). As previously reported, body weight of IRΔPOMC mice (at 12 weeks of age: 23±1 g, n=8) was not significantly different (p=0.21) from littermate controls (25±2 g, n=8). There was also no significant difference in fat pad weights (brown adipose tissue, peri-gonadal and peri-renal) between IRΔPOMC mice and littermate controls. Next, we used direct multifiber nerve recording to assess the sympathetic effects of insulin. In wild type mice, intracerebroventricular (ICV) administration of insulin (100 μU) caused a robust increase in lumbar SNA (202±36%, n=7). Surprisingly, genetic deletion of the IR from POMC neurons by loxP-Cre recombination did not alter the sympathetic response as indicated by the comparable (p=0.24 vs. littermate controls) increase in lumbar SNA in the IRΔPOMC mice in response to ICV insulin (264±40%, n=7). Ongoing studies are aimed to determine whether deletion of the IR from POMC neurons interferes with the ability of insulin to increase SNA subserving tissues other than the hindlimb. We conclude that insulin receptor signaling in POMC neurons does not mediate the lumbar sympathetic nerve activation evoked by insulin.

Sign in / Sign up

Export Citation Format

Share Document