17β-estradiol and ureteral contractility: A role for the G protein-coupled estrogen receptor

Iris Lim*, Caio Christiansen, Russ Chess-Williams

*Corresponding author for this work

Research output: Contribution to journalArticleResearchpeer-review

Abstract

The aim of this study was to investigate the unknown effects of 17β-estradiol (E2) on ureteral contractility and the receptor and mechanisms involved. By utilising isolated porcine distal ureteral strips, we observed that E2 (30 – 300μM) and a G protein-coupled estrogen receptor specific agonist G-1 (30μM) both increased the frequency of phasic contractions of the ureter (P<0.05). E2 also decreased the maximum amplitude of these contractions (P<0.05). The G protein-coupled estrogen receptor specific antagonist G-36 (10μM) reversed E2 enhancement effects on frequency, but did not alter its effects on maximum amplitude of contractile responses. Additionally, it was observed that the effects of E2 were unaltered by removing the urothelium, inhibiting nitric oxide and prostaglandin production or preventing neuronal conduction. In the presence of a potassium channel blocker, 4-aminopyridine (10μM), the effects of E2 on frequency were prevented. This finding suggests that G protein-coupled estrogen receptor mediates the increase in frequency of ureteral phasic contractions induced by E2 via activation of potassium channels, while E2 alters the amplitude of these contractions through an unknown mechanism.
Original languageEnglish
Article number174024
JournalEuropean Journal of Pharmacology
Volume899
Early online date16 Mar 2021
DOIs
Publication statusPublished - 15 May 2021

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