Aims and Methods: 

Thiazolidinediones (troglitazone, rosiglitazone), synthetic peroxisome proliferator-activated receptor (PPARg) agonists act as insulin sensitizers but beyond their antidiabetic actions they are supposed to have cardiovascular effects as well. Our first aim was to characterise the electrophysiological parameters of right ventricular papillary muscles from histidine decarboxylase knock out (HDC-KO) mice comparing with those of wild type (WT) -in control and diabetic conditions- by standard microelectrode technique. Furthermore we investigated the effects of rosiglitazone (R)(1(10^-6M)-3(3x10^-6M)-30(30x10^-6) mM) on the transmembrane action potentials.

Results: 

In HDC-KO mice statistically significant prolongation of action potential duration (APD) and decrease in maximum velocity of depolarisation (V_max) has been observed. The induced diabetes was not able to cause any further APD and V_max alterations in the KO group. Rosiglitazone caused a concentration dependent shortening of APD in both type of mice but reduced V_max only in WT mice.

Conclusion: 

The most important difference in the electrophysiological parameters (APD, V_max) between HDC-KO and WT mice could be due to the fact that HDC-KO mice are more susceptible for hyperglycaemia. The results suggest also that rosiglitazone might have direct ion channel effects (Ca^2+, K⁺) as well, but further, direct ionic current measurements need to support this explanation.