AGI July 42/1

Zavecz, James H., Orlando Bueno, Ronald E. Maloney, James M. O’Donnell, Sandra C. Roerig, and Harold D. Battarbee. Cardiac excitation-contraction coupling in the portal hypertensive rat. Am J Physiol Gastrointest Liver Physiol 279: G28–G39, 2000.— Basal contractility and responses to b-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, b-adrenoceptor-G protein coupling, and excitation-contraction coupling (ECC). Contractility (dT/dt) was reduced 30–50% in right and left ventricles, but the rate of relaxation (2dT/dt) was unaffected. Isoproterenol-induced positive inotropism was diminished, but there was no difference in ED50. The concentration-dependent increase in 2dT/dt was unaffected. Gsa and Gia expression, cholera toxinand pertussis toxin-induced ADP-ribosylation, and formation of the agonist-receptor-Gs complex were unaffected by portal vein stenosis. Of the components of ECC examined, the caffeine-sensitive sarcoplasmic reticulum Ca21 pool was reduced 35%, although the Ca21 uptake and release processes were unchanged; the apparent density of L-type Ca21 channels decreased 60% with no change in affinity; the dihydropyridine Ca21 channel agonist BAY K 8644 produced relative changes in dT/dt that were similar in both groups, suggesting normal function in the remaining Ca21 channels; and Na1/Ca21 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.