Pravastatin Relaxes Rat Thoracic Aorta via Activation of AMPK Pathway and Potassium Channels

Serdar Şahintürk

Makale detayları

Pravastatin Relaxes Rat Thoracic Aorta via Activation of AMPK Pathway and Potassium Channels

Yazarlar:

Serdar Şahintürk

Yayıncı:

Eskişehir Osmangazi University

Ana Başlıklar:

Sağlık Kurumları Yönetimi

Dergi:

Osmangazi Tıp Dergisi Vol.46 Issue 1, pp.82-92

Belge Tipi:

Makale

Yayın Tarihi:

1/2024

Belge Dili:

Türkçe

Document ID (Org No.):

2001302299

pISSN:

1305-4953

Anahtar kelimeler:

Özet:

 This study aimed to determine the functional effects and mechanisms of action of pravastatin, a cholesterol-lowering drug, in rat thoracic aorta. Vessel segments isolated from the thoracic aortas of male Wistar Albino rats were placed in chambers within an isolated tissue bath system. The resting tension was set to 1 g. After an equilibration period, the thoracic aorta rings were contracted with 10-6 M phenylephrine. Once a steady contraction was obtained, cumulative pravastatin 10-8-10-4 M was applied to the vascular rings. To identify the vasoactive effect mechanisms of pravastatin, the specified experimental protocol was repeated after incubation with specific signaling pathway inhibitors and potassium channel blockers. Pravastatin showed a concentration-dependent relaxation in precontracted rat thoracic aorta rings p0.001. The vascular relaxant effect levels of pravastatin were significantly reduced by removal of the endothelium, L-NAME application, and indomethacin incubation p0.001. Pravastatin-induced vasorelaxation levels were also significantly reduced following TEA, 4-Aminopyridine, XE-991, apamin, dorsomorphin, and anandamide administrations p0.001. However, applications of glyburide and barium chloride did not cause a statistically significant change in the vasorelaxant effect level of pravastatin p1.000. Pravastatin has a prominent vasorelaxant effect in rat thoracic aorta. Intact endothelium, nitric oxide, prostanoids, AMPK, and potassium channels BKCa, SKCa, KV, and K2p channels play a role in the vascular relaxant effect of pravastatin.

 This study aimed to determine the functional effects and mechanisms of action of pravastatin, a cholesterol-lowering drug, in rat thoracic aorta. Vessel segments isolated from the thoracic aortas of male Wistar Albino rats were placed in chambers within an isolated tissue bath system. The resting tension was set to 1 g. After an equilibration period, the thoracic aorta rings were contracted with 10-6 M phenylephrine. Once a steady contraction was obtained, cumulative pravastatin 10-8-10-4 M was applied to the vascular rings. To identify the vasoactive effect mechanisms of pravastatin, the specified experimental protocol was repeated after incubation with specific signaling pathway inhibitors and potassium channel blockers. Pravastatin showed a concentration-dependent relaxation in precontracted rat thoracic aorta rings p0.001. The vascular relaxant effect levels of pravastatin were significantly reduced by removal of the endothelium, L-NAME application, and indomethacin incubation p0.001. Pravastatin-induced vasorelaxation levels were also significantly reduced following TEA, 4-Aminopyridine, XE-991, apamin, dorsomorphin, and anandamide administrations p0.001. However, applications of glyburide and barium chloride did not cause a statistically significant change in the vasorelaxant effect level of pravastatin p1.000. Pravastatin has a prominent vasorelaxant effect in rat thoracic aorta. Intact endothelium, nitric oxide, prostanoids, AMPK, and potassium channels BKCa, SKCa, KV, and K2p channels play a role in the vascular relaxant effect of pravastatin.

 This study aimed to determine the functional effects and mechanisms of action of pravastatin, a cholesterol-lowering drug, in rat thoracic aorta. Vessel segments isolated from the thoracic aortas of male Wistar Albino rats were placed in chambers within an isolated tissue bath system. The resting tension was set to 1 g. After an equilibration period, the thoracic aorta rings were contracted with 10-6 M phenylephrine. Once a steady contraction was obtained, cumulative pravastatin 10-8-10-4 M was applied to the vascular rings. To identify the vasoactive effect mechanisms of pravastatin, the specified experimental protocol was repeated after incubation with specific signaling pathway inhibitors and potassium channel blockers. Pravastatin showed a concentration-dependent relaxation in precontracted rat thoracic aorta rings p0.001. The vascular relaxant effect levels of pravastatin were significantly reduced by removal of the endothelium, L-NAME application, and indomethacin incubation p0.001. Pravastatin-induced vasorelaxation levels were also significantly reduced following TEA, 4-Aminopyridine, XE-991, apamin, dorsomorphin, and anandamide administrations p0.001. However, applications of glyburide and barium chloride did not cause a statistically significant change in the vasorelaxant effect level of pravastatin p1.000. Pravastatin has a prominent vasorelaxant effect in rat thoracic aorta. Intact endothelium, nitric oxide, prostanoids, AMPK, and potassium channels BKCa, SKCa, KV, and K2p channels play a role in the vascular relaxant effect of pravastatin.

 Bu çalışma kolesterol düşürücü bir ilaç olan pravastatinin sıçan torasik aortundaki fonksiyonel etkilerini ve etki mekanizmalarını belirlemeyi amaçladı. Erkek Wistar Albino sıçanların torasik aortlarından izole edilen damar segmentleri, izole organ banyosu sistemindeki bölmelere yerleştirildi. Dinlenim gerimi 1 g olarak ayarlandı. Dengelenme sürecinden sonra torasik aorta halkaları 10-6 M fenilefrin ile kasıldı. Stabil bir kasılma sağlandıktan sonra damar halkalarına kümülatif 10-8-10-4 M pravastatin uygulandı. Pravastatinin vazoaktif etki mekanizmalarını belirlemek için, belirtilen deney protokolü, spesifik sinyal yolağı inhibitörleri ve potasyum kanal blokörlerinin inkübasyonundan sonra tekrarlandı. Pravastatin, önceden kasılmış sıçan torasik aort halkalarında konsantrasyona bağımlı bir gevşeme gösterdi p0,001. Endotelin çıkarılması, L-NAME uygulaması ve indometazin inkübasyonu, pravastatinin vazorelaksan etki düzeyini anlamlı ölçüde azalttı p0,001. Pravastatin kaynaklı vazorelaksasyon seviyeleri, TEA, 4-Aminopiridin, XE-991, dorsomorfin ve anandamid uygulamalarından sonra anlamlı ölçüde azaldı p0,001. Gliburid ve baryum klorür uygulamaları pravastatinin vazorelaksan etki düzeyinde istatistiksel olarak anlamlı bir değişikliğe neden olmadı p1,000. Pravastatin sıçan torasik aortunda belirgin bir vazorelaksan etkiye sahiptir. Pravastatinin vazorelaksan etkisinde sağlam endotel, nitrik oksit, prostanoidler, AMPK ve potasyum kanalları BKCa, SKCa, KV ve K2p kanalları rol oynamaktadır.

Makale detayları

Pravastatin Relaxes Rat Thoracic Aorta via Activation of AMPK Pathway and Potassium Channels

Yazarlar:

Serdar Şahintürk

Yayıncı:

Eskişehir Osmangazi University

Ana Başlıklar:

Sağlık Kurumları Yönetimi

Dergi:

Osmangazi Tıp Dergisi Vol.46 Issue 1, pp.82-92

Belge Tipi:

Makale

Yayın Tarihi:

1/2024

Belge Dili:

Türkçe

Document ID (Org No.):

2001302299

pISSN:

1305-4953

AMPK

Cholesterol

Nitric oxide

Potassium channels

Pravastatin

Rat aortaAMPK

Kolesterol

Nitrik oksit

Potasyum kanalları

Pravastatin

Sıçan aortu

Sayı

Makale detayları

Yazarlar: Serdar Şahintürk

Yayıncı: Eskişehir Osmangazi University

Ana Başlıklar: Sağlık Kurumları Yönetimi

Dergi: Osmangazi Tıp Dergisi Vol.46 Issue 1, pp.82-92

Belge Tipi: Makale

Yayın Tarihi: 1/2024

Belge Dili: Türkçe

Document ID (Org No.): 2001302299

pISSN: 1305-4953

Sayı

Yazarlar:

Serdar Şahintürk

Yayıncı:

Eskişehir Osmangazi University

Ana Başlıklar:

Sağlık Kurumları Yönetimi

Dergi:

Osmangazi Tıp Dergisi Vol.46 Issue 1, pp.82-92

Belge Tipi:

Makale

Yayın Tarihi:

1/2024

Belge Dili:

Türkçe

Document ID (Org No.):

2001302299

pISSN:

1305-4953