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

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