scholarly journals Mineralocorticoid-Induced Sodium Appetite and Renal Salt Retention: Evidence for Common Signaling and Effector Mechanisms

2014 ◽  
Vol 128 (1-2) ◽  
pp. 8-16 ◽  
Author(s):  
Yiling Fu ◽  
Volker Vallon
1977 ◽  
Vol 30 (2) ◽  
pp. 236-253 ◽  
Author(s):  
P.J. Roberts ◽  
P. Häyry

1989 ◽  
Vol 10 (12) ◽  
pp. 429
Author(s):  
David M. Ojcius ◽  
John Ding-E Young

1990 ◽  
Vol 104 (5) ◽  
pp. 742-750 ◽  
Author(s):  
Edda Thiels ◽  
Joseph G. Verbalis ◽  
Edward M. Stricker
Keyword(s):  

2011 ◽  
Vol 300 (5) ◽  
pp. R1091-R1099 ◽  
Author(s):  
S. Dayawansa ◽  
S. Peckins ◽  
S. Ruch ◽  
R. Norgren

Rats with bilateral lesions of the lateral hypothalamus (LH) fail to exhibit sodium appetite. Lesions of the parabrachial nuclei (PBN) also block salt appetite. The PBN projection to the LH is largely ipsilateral. If these deficits are functionally dependent, damaging the PBN on one side and the LH on the other should also block Na appetite. First, bilateral ibotenic acid lesions of the LH were needed because the electrolytic damage used previously destroyed both cells and axons. The ibotenic LH lesions produced substantial weight loss and eliminated Na appetite. Controls with ipsilateral PBN and LH lesions gained weight and displayed robust sodium appetite. The rats with asymmetric PBN-LH lesions also gained weight, but after sodium depletion consistently failed to increase intake of 0.5 M NaCl. These results dissociate loss of sodium appetite from the classic weight loss after LH damage and prove that Na appetite requires communication between neurons in the LH and the PBN.


2019 ◽  
Vol 19 (3) ◽  
pp. 954-955 ◽  
Author(s):  
Aleksandar Senev ◽  
Jasper Callemeyn ◽  
Evelyne Lerut ◽  
Marie‐Paule Emonds ◽  
Maarten Naesens

Sign in / Sign up

Export Citation Format

Share Document