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The Role of G Protein‐Coupled Estrogen Receptor (GPER) in the PVN of Renovascular Hypertensive Rats

It is well stablished that 17β‐estradiol acting on classic estrogen receptors is a cardiovascular protector in part via reduction of sympathetic vasomotor activity. However, there is no information regarding the G protein‐coupled estrogen receptor (GPER) actions in the paraventricular nucleus of hypothalamus (PVN) in the 2kidney‐1clip (2K‐1C) Goldblatt hypertension model. Thus, we investigated the role of GPER within the PVN on sympathetic vasomotor activity in 2K‐1C male Wistar rats. Protein expression of GPER within the PVN was evaluated by Western blot assay. Bilateral microinjection of G1 (GPER agonist) into the PVN was performed in control (C) and 2K‐1C rats, six weeks after renal clipping. Renal sympathetic nerve activity (rSNA) and mean arterial blood pressure (MAP) were recorded in urethane anesthetized rats (1,4 g/Kg, IV). A significant increase in GPER (563 ± 71% n=6) expression was found in 2K‐1C rats. G1 into the PVN induced significantly larger increase in rSNA in 2K‐1C rats (C,Δ 15.60 ± 4.885 n=5 and 2K1C,Δ 40.17 ± 4.199 n=6). However, there was no significant effect on MAP in both groups. Chronic 2K‐1C Losartan‐treated rats (30 mg/Kg/day for 7 consecutive days) significantly reduced GPER expression in the PVN (70%, n=4). The increase in GPER activity seems to contribute for the renal sympathoexcitation in renovascular hypertension. Apparently, Angiotensin II AT1 receptor is important for the PVN GPER upregulation in Goldblatt rats.