Skip to main content
. Author manuscript; available in PMC: 2014 Jul 23.
Published in final edited form as: Circulation. 2013 Jun 19;128(4):10.1161/CIRCULATIONAHA.113.003183. doi: 10.1161/CIRCULATIONAHA.113.003183

Figure 7.

Figure 7

βAR desensitization by TNFα is Gβγ independent. (A) Representative echocardiography images from Wt or βARK-ct-Tg pre- and post-TNFα treatment for 2 weeks. (B) % fractional shortening (% FS) from Wt or βARK-ct-Tg mice with or without TNFα treatment. (n=6), *p< 0.005 versus Vehicle (both Wt and βARK-ct-Tg). (C) In vitro ISO (I) (closed bars) stimulated cardiac adenylyl cyclase activity compared to vehicle (V) (open bars) in the hearts of Wt and βARK-ct-Tg mice following 2 weeks of ISO or TNFα3 treatment. (n=6), *p< 0.05 versus in vitro ISO (I) stimulated 2 weeks vehicle treated Wt or βARK-ct-Tg or 2 weeks ISO treated βARK-ct-Tg cardiac membranes. (D) Upper panel: Cardiac lysates from Wt or βARK-ct-Tg mice given a bolus of Vehicle (AA-Ascorbic Acid or Sal-saline), TNFα or ISO were immunoblotted for phospho-β2AR. Lower panel: The blot was stripped and re-probed for β-actin.