PARICALCITOL REVERSED MYOCARDIAL INJURIES INDUCED BY DEFICIENCY OF VITAMIN D RECEPTORS IN HEARTS

LILIANA ALTAMIRANO; EMILIANO DIEZ; ADRIANA CARRIÓN; AMIRA PONCE ZUMINO; WALTER MANUCHA

San Luis

Congreso; XXXII Reunión Científica Anual de la Sociedad de Biología de Cuyo; 2014

Sociedad de Biología de Cuyo

Cardiovascular diseases are often associated with chronic kidney disorders. Myocardial vitamin D receptors (VDRs) could be a link between them. Paricalcitol (vitamin D receptor activator, Pari) protects against some of those complications, but its mechanism has not been study yet. We try to determine if obstructive nephropathy (ON) linked to VDRs deficiency induce changes in structure or electrophysiologic properties (EP) and/or in the incidence of ventricular arrhythmias. Rats were underwent to ON or sham operation. Both were treated either Pari or vehicle. In some hearts we evaluated molecular and structural changes. In the other hand, in isolated hearts submitted to regional ischemia and reperfusion, EP were evaluated. ON showed a reduction in VDRs, an increase in angiotensin II type 1 receptor, fibrosis, myofibrils reduction and an increase in mitochondrial size. All these changes were reversed by Pari. Also, Pari reduced the incidence and duration of ventricular fibrillation during reperfusion, meanwhile vehicle-treated hearts maintained high incidence. Pari lengthened the action potential duration in both treated groups. Amplitude and resting potential were very similar in all groups. We concluded that the reduction in VDRs might be associated to myocardial remodeling and increasing arrhythmogenesis. Pari protects against these changes by restoring myocardial VDRs and prolonging action potencial duration.