{'fraction_non_alphanumeric': 0.03204272363150868, 'fraction_numerical': 0.022696929238985315, 'mean_word_length': 5.691964285714286, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Store‐Depletion Mediated Agonist‐Activated Contractile Responses in Rat and Human Corporal Smooth Muscle

Smooth muscle contraction is dependent on Ca2+‐influx, release of Ca2+ from intracellular stores and Ca2+‐sensitization mechanisms. Depletion of intracellular Ca2+ stores has been shown to cause Ca2+‐influx via transient receptor potential (TRP) channels. In this study we report agonist‐activated contractile responses in rat and human corporal smooth muscle when intracellular Ca2+ stores were depleted. Rat and human corporal smooth muscle strips were mounted in a myograph (DMT‐USA, Inc.) and isometric tension in response to pharmacological treatments were recorded. In the presence of caffeine, thapsigargin and nifedipine, phenylephrine (PE) and endothelin‐1 (ET1) did not evoke contraction in the absence of Ca2+. Reintroduction of extracellular Ca2+ produced concentration‐dependent contractions when increased up to 10 mM, only in the presence of PE or ET1. In rat corporal strips, these responses were completely reversed by SKF96365 and 2APB, that are known to block TRP channels. In human corporal strips, responses evoked by PE were decreased by 2APB and little affected by SKF96365, whereas those evoked by ET1 were decreased by SKF96365 but not by 2APB. This study provides functional evidence for the receptor‐activated Ca2+ influx in the presence of depleted intracellular Ca2+ stores. Characteristics of TRP channels involved in this response need systematic investigation.