Meanwhile, in IVA, vagal stimulation had no effect on the HR ( p = 0.16) and induced a significantly lower drop in SBP ( p< 0.05).

In Control, in situ vagus nerve stimulation induced progressive decrease in both the SBP ( p = 0.0001) and the HR ( p< 0.0001). Results: Ivabradine significantly increased vagal modulation and shifted the sympatho-vagal balance toward vagal dominance. The spontaneous sinus node discharge rate (SNDR) response to in vitro cholinergic receptors stimulation using carbamylcholine (10 −9–10 −6 mol/L) was also assessed in these later rats. The heart rate (HR) and systolic blood pressure (SBP) responses to in situ electrical stimulation of the vagus nerve (2–20 Hz) were assessed in 6 additional Control and 10 IVA rats. Methods: Sympathetic and parasympathetic heart rate variability parameters and right atrial HCN(1-4) RNA levels were analyzed in 6 Control and 10 ivabradine-treated male Wistar rats (IVA 3 weeks, 10 mg/kg/day). The right atrial expression of HCN genes, encoding proteins for I f, was also evaluated. We thus aimed to assess the effects of chronic ivabradine therapy on autonomic modulation and on the cardiovascular response to in situ and in vitro parasympathetic stimulation. 3Emergency Institute for Cardiovascular Diseases and Transplantation Târgu Mureş, Târgu Mureş, Romaniaīackground: The complex interactions that exist between the pacemaker current, I f, and the parasympathetic nervous system could significantly influence the course of patients undergoing chronic therapy with the I f blocker ivabradine.2Center for Advanced Medical and Pharmaceutical Research, Târgu Mureş, Romania.1University of Medicine, Pharmacy, Science and Technology “George Emil Palade” of Târgu Mureş, Târgu Mureş, Romania.Alina Scridon 1,2* Vasile Bogdan Halaţiu 1 Alkora Ioana Balan 1 Dan Alexandru Cozac 1,3 Valeriu Moldovan 1,2 Claudia Bănescu 1,2 Marcel Perian 1,2 Răzvan Constantin Şerban 3

Perian 1.1 1