Background: Chronic kidney disease is highly prevalent and is associated with cardiovascular disease. Paricalcitol protects individuals from some of the renal and cardiovascular complications associated with kidney disease. However, its electrophysiological effect during myocardial ischemia-reperfusion is currently unknown.
Aims: Using an obstructive nephropathy (ON) model, we plan to investigate the potential, structural, and functional changes of the heart that are linked to vitamin D deficiency.
Methods: The ureters of adult rats (n = 10) were unilaterally obstructed. An inductor of the vitamin D receptor (VDR) was administered for 15 days (30ng/Kg/day, ip). We evaluated histological, molecular, and biochemical parameters, as well, cardiac electrophysiological activity with ischemia-reperfusion protocol.
Results: we found changes in the action potential duration (APD) at 90% (* P<0.05 vs. C, +P<0.05 vs. O). The analysis revealed arrhythmias, ventricular tachycardia (VT), and ventricular fibrillation (VF). Arrhythmias were quantified in the following ways: 0 − sinus rhythm, 1 – premature ventricular complex, 2 - salvos, 3 - no sustained VT, and 4 – sustained VT or VF (>30 seconds). * P<0.05 vs. C, +P<0.05 vs. O. Of interest was the finding that appears to prolong Pari ischemia DPA in both the controls and the obstructed animals. Also, a significant bradycardia was established in the ischemic phase of the animals obstructed with Pari, which reversed completely during reperfusion. In hearts from ON model animals, we found high AT1 expression and marked low VDR expression; these changes were reversed by paricalcitol treatment.
Conclusions: The reduction of VDR expression in ON hearts could be related to increased arrhythmogenesis. The recovery induced by paricalcitol could protect against ventricular fibrillation by the lengthening of the action potential. Further studies will be necessary to elucidate these interesting kidney-heart interactions.