Cardiac excitation-contraction coupling in the portal hypertensive rat

Basal contractility and responses to β-adrenoceptor activation are compromised in hearts from rats with chronic portal vein stenosis. Here we report the effect of partial ligation of the portal vein on myocardial G protein expression, β-adrenoceptor-G protein coupling, and excitation-contraction coupling (ECC). Contracility (dT/dt) was reduced 30-50% in right and left ventricles, but the rate of relaxation (-dT/dt) was unaffected. Isoproterenol-induced positive inotropism was diminished, but there was no difference in ED₅₀. The concentration-dependent increase in -dT/dt was unaffected. G(s)α and G(i)α expression, cholera toxin- and pertussis toxin-induced ADP-ribosylation, and formation of the agonist-receptor-G(s) complex were unaffected by portal vein stenosis. Of the components of ECC examined, the caffeine-sensitive sarcoplasmic reticulum Ca²⁺ pool was reduced 35%, although the Ca²⁺ uptake and release processes were unchanged; the apparent density of L-type Ca²⁺ channels decreased 60% with no change in affinity; the dihydropyridine Ca²⁺ channel agonist BAY K 8644 produced relative changes in dT/dt that were similar in both groups, suggesting normal function in the remaining Ca²⁺ channels; and Na⁺/Ca²⁺ exchange was reduced 50% in the portal vein stenosis group. These data suggest that the effect of portal vein stenosis on the myocardium is the result of alterations to ECC.