Refractory period (sex) for treating sexual dysfunction. Sildenafil, used in the treatment of erectile dysfunction, was found in one scientific study to have caused "a decreased postejaculatory erectile refractory time (3.2 ± 0.7 vs. 6.4 ± 0.7 minutes)" in men diagnosed with premature ejaculation. It is additionally proposed that the gonadotropin inhibitory hormone (GnIH), which is considered to inhibit the hypothalamic-pituitary-gonadal axis and sexual functions causes refractoriness of the post-ejaculatory refractory period. This hypothesis also supports the increase of oxytocin and prolactin after orgasm in accordance with the previous studies. One alternative theory explains the male refractory period in terms of a peripheral
KCNE2 less milk (hypothyroidism of the dams impairs milk ejection), the milk they receive is deficient in T, and they themselves cannot adequately transport iodide into the thyroid. "Kcne2"-/- pups exhibit stunted growth, alopecia, cardiomegaly and reduced cardiac ejection fraction, all of which are alleviated by thyroid hormone supplementation of pups or dams. Surrogating "Kcne2"-/- pups with "Kcne2"+/+ dams also alleviates these phenotypes, highlighting the influence of maternal genotype in this case. As observed for hERG mutations, KCNE2 loss-of-function mutations are associated with inherited LQTS, and hERG-KCNE2 channels carrying the mutations show reduced activity compared to wild-type channels. In addition, some