Figure 4.

Blockade of nuclear export inhibits α1‐AR‐mediated contractility in adult cardiac myocytes. A, Sarcomere dynamics and (B) Ca²⁺ transients were measured in WT cardiac myocytes pretreated with vehicle or leptomycin B (lepB; 18.5 μmol/L, right) before and 5 minutes after phenylephrine (PE) treatment (10 μmol/L of PE, 2 μmol/L of timolol in all conditions). Single‐twitch contractions or calcium transients are shown at 5 minutes after the addition of PE. Averaged data for percent (%) sarcomere shortening and fold change in calcium (ΔCa²⁺) at 5 minutes after PE are presented as mean±SEM from 21 WT cardiac myocytes treated with vehicle and 29 WT cardiac myocytes treated with lepB from 10 different cultures. C, cTnI phosphorylation at Thr144 measured by Western blot from WT cardiac myocytes pretreated with vehicle or leptomycin B followed by PE (20 μmol/L, 15 minutes). Quantitation of cTnI phosphorylation at Thr144 is presented as mean±SEM from 8 different cultures. All data were analyzed by 2‐way ANOVA with repeated measures and Bonferroni's post‐test. Percent sarcomere shortening, P=NS; ΔCa²⁺, P=NS; cTnI phosphorylation at Thr144, P=0.0425. Significant comparisons identified by Bonferroni's post‐test are indicated as P<0.05. ANOVA indicates analysis of variance; cTnI, cardiac troponin I; WT, wild type; α1‐ARs, α1‐adrenergic receptors.