Key result
Chronic exposure to low doses of estradiol-17ß significantly increased average mean arterial pressure to 104.37 mmHg compared to 99.04 mmHg in control rats.
Why the study?
Does chronic exposure to low doses of estradiol-17β increase blood pressure in young female rats via central Endothelin-1?
Does chronic exposure to low doses of estradiol-17β increase blood pressure in young female rats via central Endothelin-1?
Chronic exposure to low-dose estradiol increases blood pressure in young female rats, which is associated with the upregulation of central endothelin-1 and ETA receptors.
Answers are grounded in this paper and cite their sources.
May warrant caution interpreting estrogen effects on BP; hypothesis-generating for central ET-1 mediation in young females.
Previously, we demonstrated that chronic exposure to low levels of estradiol-17β (E2) increases mean arterial pressure (MAP) in young female Sprague-Dawley (SD) rats, however, the underlying mechanisms are unclear. Since endothelin-1 (ET-1) is implicated in blood pressure (BP) regulation, we hypothesized that E2’s effects on MAP are mediated through central ET-1. To test this, young female SD rats were either sham implanted or implanted s.c. with slow-release E2 pellets (20 ng/day for 90 days). BP was monitored by telemetry. After 75 days of E2 exposure, ET A antagonist or vehicle was administered i.c.v. After 90 days of E2 exposure, rats were sacrificed, and the paraventricular nucleus (PVN) and rostral ventrolateral medulla (RVLM) were microdissected for gene expression and protein analysis of ET-1 and its receptors. E2 exposure increased MAP after pellet implantation. Gene expression of ET-1 and ET A but not ET B receptors were upregulated in the PVN and RVLM of E2 treated animals. Further, the protein levels of ET A receptor were also increased in the PVN of E2 treated animals. However, i.c.v. infusion of the ET A antagonist did not completely block the increase in blood pressure. Our results suggest that increases in central ET-1 activity could possibly play a role in chronic E2-induced increase in BP but further studies are needed to completely understand the contribution of ET-1 in this phenomenon.
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Subramanian et al. (2017) studied Healthy (to study E2-induced hypertension). Estradiol-17ß (E2) vs. Sham-implanted was evaluated on Average mean arterial pressure (MAP) over 75 days (p=0.0057). Chronic exposure to low doses of estradiol-17ß significantly increased average mean arterial pressure to 104.37 mmHg compared to 99.04 mmHg in control rats.
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