scholarly journals Effects of glucagon and noradrenaline on the blood flow through brown adipose tissue in temperature-acclimated rats.

1983 ◽  
Vol 33 (3) ◽  
pp. 367-376 ◽  
Author(s):  
Takehiro YAHATA ◽  
Yoshiaki HABARA ◽  
Akihiro KUROSHIMA
Keyword(s):  
Blood Flow ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Brown Adipose ◽  
Flow Through

Involvement of nitric oxide in noradrenaline-induced increase in blood flow through brown adipose tissue

Life Sciences ◽  
1994 ◽  
Vol 54 (1) ◽  
pp. 17-25 ◽  
Author(s):  
Tomoaki Nagashima ◽  
Hiroshi Ohinata ◽  
Akihiro Kuroshima
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Brown Adipose ◽  
Flow Through

SR59230A, a beta-3 adrenoceptor antagonist, inhibits ultradian brown adipose tissue thermogenesis and interrupts associated episodic brain and body heating

2011 ◽  
Vol 301 (4) ◽  
pp. R987-R994 ◽  
Author(s):  
Youichirou Ootsuka ◽  
Keerthi Kulasekara ◽  
Rodrigo Cunha de Menezes ◽  
William W. Blessing
Keyword(s):  
Blood Flow ◽  
Adipose Tissue ◽  
Body Temperature ◽  
Brown Adipose Tissue ◽  
Neural Control ◽  
Substantial Contribution ◽  
Artery Blood Flow ◽  
Body Temperatures ◽  
Tail Artery ◽  
Brown Adipose

Brown adipose tissue (BAT) thermogenesis occurs episodically in an ultradian manner approximately every 80–100 min during the waking phase of the circadian cycle, together with highly correlated increases in brain and body temperatures, suggesting that BAT thermogenesis contributes to brain and body temperature increases. We investigated this in conscious Sprague-Dawley rats by determining whether inhibition of BAT thermogenesis via blockade of beta-3 adrenoceptors with SR59230A interrupts ultradian episodic increases in brain and body temperatures and whether SR59230A acts on BAT itself or via sympathetic neural control of BAT. Interscapular BAT (iBAT), brain, and body temperatures, tail artery blood flow, and heart rate were measured in unrestrained rats. SR59230A (1, 5, or 10 mg/kg ip), but not vehicle, decreased iBAT, body, and brain temperatures in a dose-dependent fashion (log-linear regression P < 0.01, R2 = 0.3, 0.4, and 0.4, respectively, n = 10). Ultradian increases in BAT, brain, and body temperature were interrupted by administration of SR59230A (10 mg/kg ip) compared with vehicle, resuming after 162 ± 24 min (means ± SE, n = 10). SR59230A (10 mg/kg ip) caused a transient bradycardia without any increase in tail artery blood flow. In anesthetized rats, SR59230A reduced cooling-induced increases in iBAT temperature without affecting cooling-induced increases in iBAT sympathetic nerve discharge. Inhibition of BAT thermogenesis by SR59230A, thus, reflects direct blockade of beta-3 adrenoceptors in BAT. Interruption of episodic ultradian increases in body and brain temperature by SR59230A suggests that BAT thermogenesis makes a substantial contribution to these increases.

Sign in / Sign up

Export Citation Format

Share Document