We identified 3‐fold differences among inbred rat strains in STaH (Physiol Genomics 43: 758, 2011). We hypothesized that a protein of the caspase recruitment domain (CARD9) might be a specific cellular mediator associated with these differences. CARD9 is a known activator of nuclear factor κβ (JBC 275: 41082, 2000), a transcription factor that mediates both protective and detrimental effects on myocardial function (Clin Sci 118: 593, 2010). To test this hypothesis, we measured CARD9 mRNA levels using real‐time PCR in cardiac tissue in three inbred rat strains [Dark Agouti (DA), Fawn Hooded Hypertensive (FHH), and Brown Norway (BN)] divergent in STaH (DA = FHH >; BN). Rats from each strain were randomized to three treatment groups (n=5/group): controls without surgery (C); surgically catheterized rats (Cath); and catheterized and hemorrhaged rats (Bled). Surgeries were conducted ~ 24 hr prior to hemorrhage and tissue collections. Tissues were collected 30 min after start of a 26 min ~47% hemorrhage, or 30 min post handling in C and Cath rats. CARD9 mRNA was increased 3 to 25‐fold in DA vs BN or FHH rats (P < 0.01). Hemorrhage had no effect on CARD9 mRNA in any strain, but in DA CARD9 mRNA decreased in Cath vs C rats (P<0.05). These data indicate inbred rat strain‐dependent differences in cardiac CARD9 mRNA. High CARD9 mRNA in DA rats could influence cardiac responses to hemorrhage although not altered by hemorrhage itself.