17β Estradiol relaxes tension in male guinea pig gallbladder strips

In this study we have shown that 17β estradiol (E 2 ) caused relaxation of male guinea pig gallbladder strips precontracted with either 1nM cholecystokinin octapeptide (CCK) or 40mM KCl. E 2 relaxation was concentration dependent in both cases. The purpose of this study was to determine whether E 2 relaxation was due to inhibition of intracellular Ca 2+ release by IP 3 or extracellular Ca 2+ entry. Paired t‐tests were used. The KCl and CCK produced similar amounts of tension (0.84±0.04 vs. 0.88±0.05g, n=7). The E 2 induced relaxation after CCK was significantly (p<0.001; 46.1±10.8 vs. 74.9±8.1%, n=7) less than observed with KCl. 2‐APB (125 μM), significantly (p<0.001; 0.87±0.06 vs. 0.41±0.07g, n=4) decreased CCK induced tension, and significantly (p<.0.01; 57.5±5.5 vs. 71.2±5.6%, n=4) increased E 2 induced relaxation. Similar results were observed when KCl was used with 2‐APB (p<0.001; 0.8±0.07 vs. 0.61±0.06g, n=4). The E 2 induced relaxation was increased in the presence of 2‐APB (p<0.01; 73.7±8.3 vs. 100.2±5.5%, n=3). E 2 induced relaxation of KCl induced tension suggested that the E 2 induced relaxation is mediated by inhibiting extracellular Ca 2+ entry. The use of 2‐APB and the increase in E 2 induced relaxation supports this conclusion. E 2 relaxed CCK induced tension; 2‐APB increased the E 2 relaxation. E 2 induced relaxation is primarily mediated by blocking extracellular Ca 2+ entry.