{'fraction_non_alphanumeric': 0.04282315622521808, 'fraction_numerical': 0.023790642347343377, 'mean_word_length': 5.677248677248677, '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}}
Muscarinic receptor subtype (M1) identification on rabbit pulmonary vascular endothelium in vivo.

We have investigated the presence of M1-subtype muscarinic receptors on pulmonary vascular endothelium in vivo. Utilizing multiple indicator-dilution techniques, we studied [3H]-pirenzepine ([3H]-PNZ; a selective M1 receptor antagonist) binding during a single transpulmonary pass in anesthetized, artificially ventilated rabbits, before and after administration of 4.3 mumol/kg of the nonselective muscarinic receptor antagonist atropine. [14C]-Dextran (MW = 70,000-90,000) served as the intravascular indicator. Before atropine administration, approximately 20% of [3H]-PNZ was lost (i.e., presumed bound to PNZ-specific and nonspecific sites) during a single pass through the pulmonary microvasculature. A significant decrease in [3H]-PNZ binding occurred 90 min after atropine (to approximately 60% of total initial binding), but not after saline, reflecting the loss of specific binding to M1 receptors. These data are in support of previous findings from our laboratory indicating a pressor response to M1 receptor stimulation in the rabbit pulmonary circulation as well as an endothelium-dependent contractile response to M1 receptor stimulation in vitro.