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

Raviye Özen Koca; Zülfikare Işık Solak Görmüş; Hatice Solak; Gülnur Akdoğan

Article Details

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

Authors:

Raviye Özen Koca | Zülfikare Işık Solak Görmüş | Hatice Solak | Gülnur Akdoğan

Publisher:

Harran University

Main Topics:

Sistem Fizyolojisi | Tıbbi Fizyoloji (Diğer)

Journal:

Harran Üniversitesi Tıp Fakültesi Dergisi Vol.22 Issue 3, pp.506-514

Document Type:

Article

Publication Date:

9/2025

Document Language:

English

Document ID (Org No.):

2001352418

pISSN:

1304-9623

Keywords:

Abstract:

 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.

 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.

 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.

 Amaç: Depresyon kardiyovasküler hastalığı olanlarda yaygın olarak görülmektedir. En sık kullanılan antidepresan ilaçlar olan serotonin geri alım inhibitörlerinin SSRIlar potansiyel kardiyovasküler etkilerine ilişkin klinik veriler tartışmalıdır. Mevcut çalışmada sitalopram ve paroksetinin sıçanların endotel sağlam ve hasarlı aort dokularındaki kas kontraksiyonuna etkilerinin karşılaştırılması hedeflenmiştir. Materyal ve Metod: Endotel Sağlam Aort Paroksetin HEParox, Endotel Hasarlı Aort Paroksetin DEParox, Endotel Sağlam Aort Sitalopram HECital, Endotel Hasarlı Aort Sitalopram DECital grubu olarak ayrılan 12 adet erkek Wistar Albino cinsi sıçandan torasik aort doku kesitleri çıkarıldı. Dokular izole organ banyosu sistemine yerleştirildi. Endotel sağlam gruplara 10-6 M fenilefrin PE uygulanarak maksimum kasılma elde edildi. Endotel hasarlı gruplardaki aort kesitlerine endotel hasarı oluşturulup 10-6 M PE verildi. 10-6 M asetilkolin Ach uygulanarak endotel hasarı kontrol edildikten sonra ikinci doz PE uygulanarak maksi-mum kasılmalar kaydedildi. Kasılmalar plato çizince ilgili gruplara 10-8  10-3 M paroksetin ve sitalopram dozları kümülatif olarak uygulandı. PE verilmeden önceki 10. dakika ile verildikten sonraki 10. dakika ve her ilaç dozu uygulamasından sonraki 5 dakika-lık sürede meydana gelen kas gerim parametreleri değerlendirildi. Çalışmanın istatistiksel analizleri R 4.3.1 programıyla gerçek-leştirildi. Bulgular: Paroksetin ve sitalopram aort kasılmasında zamana bağlı önemli ölçüde farklı değişikliklere neden oldu; sitalopram, hem sağlıklı hem de hasarlı endotelde paroksetinden daha güçlü bir inhibitör etki gösterdi p  .001. Gerim değerlerinin zamana göre değişimi grup içinde ikişerli karşılaştırıldığında anlamlı farklılıklar saptandı p  .05. Zaman içi gerim değerleri gruplar arasında karşılaştırıldığında anlamlı farklılıklar tespit edildi p  .001. Sonuç: Paroksetin ve sitalopram endoteli sağlam aort dokusunda doza bağlı baskılanmış bir kontraktil yanıt meydana getirmiş-tir. Endoteli hasarlı aort dokusunda ise yalnız sitalopram baskılanmış bir kontraktil yanıt meydana getirmiştir. Bu sonuç sitalop-ramın endotelden bağımsız, paroksetinin ise endotele bağımlı bir şekilde etkinlik gösterdiğini ortaya koymaktadır. Paroksetin ve sitalopram gibi sık tercih edilen SSRI türü antidepresan ilaçların kardiyovasküler hastalık durumlarındaki kullanımlarının güvenli-ği ve etkinliği hakkında daha fazla araştırmaya ihtiyaç bulunmaktadır.

Article Details

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

Authors:

Raviye Özen Koca | Zülfikare Işık Solak Görmüş | Hatice Solak | Gülnur Akdoğan

Publisher:

Harran University

Main Topics:

Sistem Fizyolojisi | Tıbbi Fizyoloji (Diğer)

Journal:

Harran Üniversitesi Tıp Fakültesi Dergisi Vol.22 Issue 3, pp.506-514

Document Type:

Article

Publication Date:

9/2025

Document Language:

English

Document ID (Org No.):

2001352418

pISSN:

1304-9623

Aorta

Cardiovascular

Contraction

Paroxetine

Citalopram.Aort

Kardiyovasküler

Kasılma

Paroksetin

Sitalopram.

Issues

Article Details

Authors: Raviye Özen Koca | Zülfikare Işık Solak Görmüş | Hatice Solak | Gülnur Akdoğan

Publisher: Harran University

Main Topics: Sistem Fizyolojisi | Tıbbi Fizyoloji (Diğer)

Journal: Harran Üniversitesi Tıp Fakültesi Dergisi Vol.22 Issue 3, pp.506-514

Document Type: Article

Publication Date: 9/2025

Document Language: English

Document ID (Org No.): 2001352418

pISSN: 1304-9623

Issues

Authors:

Raviye Özen Koca | Zülfikare Işık Solak Görmüş | Hatice Solak | Gülnur Akdoğan

Publisher:

Harran University

Main Topics:

Sistem Fizyolojisi | Tıbbi Fizyoloji (Diğer)

Journal:

Harran Üniversitesi Tıp Fakültesi Dergisi Vol.22 Issue 3, pp.506-514

Document Type:

Article

Publication Date:

9/2025

Document Language:

English

Document ID (Org No.):

2001352418

pISSN:

1304-9623