Vasorelaxant and Antihypertensive Effects of Bergenin on Isolated Rat Aorta and High Salt-Induced Hypertensive Rats

Taseer Ahmad; Rahila Qayyum; Taous Khan; Mater H Mahnashi; Mohammed M Jalal; Malik A Altayar; Osama M Alshehri; Abdul Jabbar Shah

doi:10.1155/2022/4886193

Vasorelaxant and Antihypertensive Effects of Bergenin on Isolated Rat Aorta and High Salt-Induced Hypertensive Rats

Evid Based Complement Alternat Med. 2022 Nov 22:2022:4886193. doi: 10.1155/2022/4886193. eCollection 2022.

Authors

Taseer Ahmad^{1

2}, Rahila Qayyum¹, Taous Khan¹, Mater H Mahnashi³, Mohammed M Jalal⁴, Malik A Altayar⁴, Osama M Alshehri⁵, Abdul Jabbar Shah¹

Affiliations

¹ Department of Pharmacy, COMSATS University Islamabad, Abbottabad Campus, University Road, Abbottabad, KPK 22060, Pakistan.
² Laboratory of Cardiovascular Research and Integrative Pharmacology, College of Pharmacy, University of Sargodha, Sargodha 40100, Pakistan.
³ Department of Pharmaceutical Chemistry, School of Pharmacy, Najran University, Najran, Saudi Arabia.
⁴ Department of Medical Laboratory Technology, Faculty of Applied Medical Sciences, University of Tabuk, Tabuk, Saudi Arabia.
⁵ Department of Clinical Laboratory Sciences, Collage of Applied Medical Science, Najran University, Najran, Saudi Arabia.

Abstract

Bergenin is a phenolic glycoside that has been reported to be present in some medicinal plants which are traditionally used for their antihypertensive actions. So, bergenin was investigated for antihypertensive and vasorelaxant experiments in a rat model. Bergenin produced a significant fall in the mean arterial pressure (MAP) of rats. To explore the involvement of NO and muscarinic receptors, rats were pretreated with L-NAME and atropine in-vivo. The L-NAME did not change significantly the effect of bergenin on MAP excluding the involvement of NO. Unlike the L-NAME, atropine pretreatment reduced the effect of bergenin on MAP, indicating the role of muscarinic receptors. In in-vitro study, the bergenin produced endothelium-dependent (at lower concentrations) and independent (at higher concentrations) vasorelaxation, which was attenuated significantly in the presence of atropine and indomethacin but not with L-NAME. While a partial response was observed against K⁺-induced contractions. This was further confirmed when bergenin partly shifted the CaCl₂-CRCs toward right. Bergenin also suppressed the PE peak formation, indicating the antagonist effect against the release of Ca²⁺. Moreover, the bergenin-induced vasorelaxant response was not markedly attenuated with TEA, while significantly ablated with 4-AP and BaCl₂. In conclusion, the antihypertensive effects of bergenin are due to Ca²⁺ channel blockade, K⁺ channels activation, and muscarinic receptor-linked vasodilation.