{'fraction_non_alphanumeric': 0.03182827535159141, 'fraction_numerical': 0.007401924500370096, 'mean_word_length': 5.035714285714286, '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}}
Cholecystokinin causes contraction of the pupillary sphincter in monkeys but not in cats, rabbits, rats and guinea-pigs: antagonism by lorglumide.

The effects of intracameral injections of cholecystokinin (CCK) on the pupil size were determined in monkeys, cats, rabbits, rats and guinea-pigs. In animals under muscarinic cholinergic blockade, CCK caused miosis in monkeys but not in the other species investigated. In monkeys CCK-8 was more potent than CCK-33, which was, however, much more potent than non-sulphated CCK-8. These observations indicate that peripheral type A receptors mediated the miotic response. The effect of CCK-8 was not appreciably influenced by pretreatment with indomethacin, 3 mg kg-1 body wt, indicating that prostaglandins were not involved in the response. Nerve blockade with 0.9 micrograms tetrodotoxin intracamerally had no clear effect on the dose-response relationship for CCK-8. The effect of the peptide thus seems to be directly on receptors on the pupillary sphincter muscle. Pretreatment with lorglumide caused a dose-dependent rightward shift of the dose-response curve, indicating competitive antagonism. The results indicate that in monkeys, but not in rabbit, cats, rats and guinea-pigs, CCK is a potent miotic with a direct effect on the pupillary sphincter mediated by type A CCK receptors on the muscle.