{'fraction_non_alphanumeric': 0.015957446808510637, 'fraction_numerical': 0.005319148936170213, 'mean_word_length': 6.776859504132231, '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}}
Pharmacomechanical coupling in smooth muscle may involve phosphatidylinositol metabolism.

Cholinergic contraction of canine trachealis muscle, a contraction that primarily utilizes membrane potential-independent mechanisms for activating contractile proteins (pharmacomechanical coupling), is associated with a decline in the phosphatidylinositol pool, an increase in the phosphatidic acid and diacylglycerol pools, and an increased incorporation of 32PO4 into phosphatidylinositol. We found that these changes occur during development of the contraction and during maintenance of tension and are independent of membrane depolarization or increases in cytosolic Ca2+ concentration. These findings suggest that phosphatidylinositol turnover may be part of a receptor transduction process controlling receptor-operated Ca2+ channels or other membrane potential-independent mechanisms involved in pharmacomechanical coupling in smooth muscle.