How Do Paroxetine and Citalopram Affect the Force of Contraction in Endothelially Investigated and Damaged Aortic Tissue?

Background: Depression is common in patients with cardiovascular disease. Clinical data on the potential cardiovascular effects of the most commonly used antidepressant drugs, serotonin reuptake inhibitors (SSRI), are controversial. The present study aimed to compare the effects of citalopram and paroxetine on muscle contraction in endothelial intact and damaged aortic tissues of rats. Materials and Methods: Thoracic aortic tissue sections were removed from 12 male Wistar Albino rats divided into Healthy Endothelium Aorta Paroxetine (HEParox), Damaged Endothelium Aorta Paroxetine (DEParox), Healthy Endothelium Aorta Citalopram (HECital), Damaged Endothelium Aorta Citalopram (DECital) groups. The tissues were placed in the isolated organ bath system. Maximum contraction was obtained by adding 10-6 M phenylephrine (PE) to the endothelium intact groups. Endot-helial damage was created in the aorta sections in the endothelium damaged groups and 10-6 M PE was given. After controlling the endothelial damage by adding 10-6 M acetylcholine (Ach), a second dose of PE was added and maximum contractions were recorded. When the contractions reached a plateau, cumulative doses of 10-8 – 10-3 M paroxetine and citalopram were added to the relevant groups. Muscle tension parameters occurring 10 minutes before PE addition, 10 minutes after addition, and 5 minutes after each drug dose were evaluated. Statistical analyses of the study were performed with the R 4.3.1 program. Results: Paroxetine and citalopram caused significantly different time-dependent changes in aortic contraction, with citalopram exerting a stronger inhibitory effect than paroxetine in both healthy and damaged endothelium (p < .001). When the change in tension values over time was compared in pairs within the group, significant differences were detected (p < .05). When the tension values over time were compared between the groups, significant differences were detected (p < .001). Conclusions: Paroxetine and citalopram produced a dose-dependent suppressed contractile response in endothelial-intact aortic tissue. In endothelial-damaged aortic tissue, only citalopram produced a suppressed contractile response. This result demonst-rates that citalopram is endothelium-independent, whereas paroxetine is endothelium-dependent. More research is needed on the safety and efficacy of frequently preferred SSRI antidepressant drugs such as paroxetine and citalopram in cardiovascular disease conditions