Role of corticotropin-releasing factor on bladder function in rats with psychological stress

2019 ◽  
Vol 18 (1) ◽  
pp. e708
Author(s):  
M. Seki ◽  
X-M. Zha ◽  
H. Ito ◽  
Y. Aoki ◽  
Y. Matsuta ◽  
...  
2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Masaya Seki ◽  
Xin-Min Zha ◽  
So Inamura ◽  
Minekatsu Taga ◽  
Yosuke Matsuta ◽  
...  

1998 ◽  
Vol 275 (5) ◽  
pp. R1461-R1467 ◽  
Author(s):  
Tetsuya Ando ◽  
Jean Rivier ◽  
Hitoshi Yanaihara ◽  
Akira Arimura

We previously reported the elevation of plasma interleukin (IL)-6 activity in response to immobilization stress in rats. To investigate the role of peripheral corticotropin-releasing factor (CRF) in this response, we examined the effects of CRF antagonists on immobilization-induced IL-6 response. Intravenous pretreatment with either [d-Phe12,Nle21,38,CαMeLeu37]-anti-human rat (h/r) CRF12—41(1.5 mg/kg) or cyclo(30—33)[d-Phe12, Nle21,38,Glu30,Lys33]-h/rCRF12—41(Astressin, 0.5 mg/kg) attenuated the IL-6 response to immobilization, which confirmed our previous finding that systemic administration of an antiserum against CRF blocked this response. In addition, an intraperitoneal injection of h/rCRF (100 μg/kg) or rat urocortin (10 and 100 μg/kg) increased the plasma IL-6 activity, mimicking the response to immobilization. An intravenous injection of h/rCRF (100 μg/kg) also elevated plasma IL-6 in adrenalectomized rats. These findings suggest that peripheral CRF mediates the plasma IL-6 elevation in response to immobilization.


2011 ◽  
Vol 63 (1) ◽  
pp. 257-258
Author(s):  
Carmen Lasheras ◽  
Ana González-Cuello ◽  
Maria Victoria Milanés ◽  
Maria Luisa Laorden

1993 ◽  
Vol 265 (4) ◽  
pp. R834-R839 ◽  
Author(s):  
T. Nakamori ◽  
A. Morimoto ◽  
N. Murakami

We investigated the role of central corticotropin-releasing factor (CRF) in the development of cardiovascular and thermal responses induced by stress or by interleukin-1 beta (IL-1 beta) in free-moving rats. Intracerebroventricular (icv) injection of alpha-helical CRF9-41 (10 micrograms), a CRF receptor antagonist, significantly attenuated hypertension, tachycardia, and a rise in body temperature induced by cage-switch stress, a mild stress. However, icv injection of alpha-helical CRF9-41 (10 micrograms) had no effect on hypertension, tachycardia, or fever induced by intraperitoneal (ip) injection of IL-1 beta (2 micrograms/kg) or icv prostaglandin E2 (PGE2, 100 ng). In contrast, icv injection of alpha-helical CRF9-41 (10 micrograms) significantly attenuated hypertension, tachycardia, or fever induced by icv injection of IL-1 beta (20 ng). The present results suggest that central CRF has an important role in the development of the cage-switch stress-induced responses, but it does not seem to contribute to the hypertension, tachycardia, and fever induced by ip IL-1 beta or by central PGE2. However, it is possible that when IL-1 beta directly acts on the central nervous system, some of its actions are mediated by central CRF.


2012 ◽  
Vol 49 ◽  
pp. 532-535 ◽  
Author(s):  
Andrea J. Day ◽  
Kate Brasher ◽  
Robert S. Bridger

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