Estrogen Protects Vasomotor Functions in Rats During Catecholamine Stress

Frontiers in Cardiovascular Medicine

Liting Yang¹  Mingjin Shi¹  Jeremiah Ong'achwa Machuki¹  Hong Sun¹  Chenfei Li¹  Qi Sun¹  Gabriel Komla Adzika¹  Lin Zhang² 

[1] Department of Physiology, Xuzhou Medical University, Xuzhou, China;Department of Physiology, Xuzhou Medical University, Xuzhou, China;Institute of Cardiovascular Disease Research, Xuzhou Medical University, Xuzhou, China;

关键词: estrogen;    catecholamine stress;    vasomotor function;    nitric oxide;    endothelin-1;   

DOI  :  10.3389/fcvm.2021.679240

来源: Frontiers

【 摘 要 】

The incidence of dysfunctional vasomotor diseases has mostly occurred in postmenopausal women but not in premenopausal women. Hence, this study sought to investigate the impact of estrogen deficiency during catecholamine stress on vasomotor function. Also, attempts were made to utilize estrogen replacement therapy to mitigate the adverse effects (pathological remodeling) of stress on the aortic vessels to preserve vasomotor functions. To do this, female Sprague-Dawley (SD) rats were ovariectomized (OVX) along with sham operations (Sham). Day 14 after OVX operation, 17-estradiol (E2) was subcutaneously implanted (OVX+E2). Day 35 after operation, stress was induced by isoproterenol (ISO) subcutaneous injections. Clinically relevant blood pressure indexes (systolic, diastolic, and mean atrial blood pressures) were assessed in the rats. Aortic vascular ring tensions were assessed in vitro to ascertain the impact of E2 on their vasomotor function. Aortic vascular rings (AVRs) from OVX+ISO exhibited a significant increase in contractility in response to phenylephrine than AVRs isolated from Sham+ISO rats. Also, sera levels of nitric oxide (NO) and endothelin-1 (ET-1) and the expression of p-eNOS/eNOS from vascular tissues were ascertained. We demonstrate that, during stress, E2 prevented excessive weight gain and OVX rats had higher blood pressures than those in the Sham group. Further, we showed that E2 decreases ET-1 expressions during stress while upregulating NO expressions via enhancing eNOS activities to facilitate vasomotor functions. Finally, histological assessment revealed the E2 treatments during stress preserved vasomotor functions by preventing excessive intima-media thickening and collagen depositions in the aortic vascular walls.

【 授权许可】

CC BY