Abstract
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.
Highlights
Premenopausal women have a lower incidence of vascular disease than men of the same age, but this sexual advantage disappears after menopause [1, 2]
The morphometrics results obtained demonstrate that, in the normal state, the presence of endogenous estrogen (E2Endo) in the sham operations (Sham) group and the OVX supplemented with exogenous estrogen (E2Exo) in the OVX+E2 group influenced reduction in heart weights compared with the OVX group, there was not any statistical significance among the groups
In terms of body weights, it was observed that the deficiency of E2 in OVX rats encourages weight gain significantly compared to the Sham and OVX+E2
Summary
Premenopausal women have a lower incidence of vascular disease than men of the same age, but this sexual advantage disappears after menopause [1, 2]. Studies have shown that postmenopausal women have an increased response to stress, and estrogen supplementation can reduce this response [5, 6] This suggests that stress and estrogen deficiency are both risk factors for vascular disease in postmenopausal women. Research findings over the last decade have demonstrated that by supplementing estrogen during the menopausal period, the adverse effects of catecholamine stress on the cardiovascular system (CVS) are subdued [7, 8]. These findings suggested that experiencing chronic stress during an estrogen deficiency period may be risk factors that facilitate vascular disease pathogenesis in menopausal women.
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