{'fraction_non_alphanumeric': 0.0347877358490566, 'fraction_numerical': 0.024174528301886794, 'mean_word_length': 5.40377358490566, '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}}
Prejunctional prostaglandin receptors in the human iris-ciliary body.

Prostaglandins (PGs) of the E series have been shown to modulate sympathetic neurotransmitter release in a variety of peripheral tissues and organs, including the eye. In this study, we evaluated the inhibitory effects of a series of naturally-occurring and synthetic PGs on field stimulation-evoked release of 3H-norepinephrine (3H-NE) from isolated, superfused segments of human iris-ciliary body. Field-stimulated 3H-NE secretion was calcium-dependent, blocked by selective inhibitors of voltage-sensitive calcium and sodium channels, and originated from a desipramine-sensitive transmitter pool. Evoked 3H-NE release was inhibited in a concentration-dependent manner by PGE2 (EC50 = 45 nM) and several closely related compounds with the following rank order of potency: sulprostone greater than 16,16-dimethyl-PGE2 greater than PGE2 greater than 11-deoxy-PGE1. By contrast, PGF2 alpha was relatively inactive (EC50 greater than 10 microM) in this system. None of the above compounds significantly modified spontaneous 3H-NE efflux. PGE2-mediated inhibition was not antagonized by the selective prostanoid EP1-receptor antagonists AH 6809 (10 microM) or SC-19220 (30 microM), nor did these agents alone affect basal or field-stimulated 3H-NE release. The results suggest that human ocular sympathetic nerves possess inhibitory PG receptors which have the pharmacological properties of the EP3 subtype. These receptors may play a role in local feedback regulation of sympathetic transmission in the iris-ciliary body, and may contribute to symptoms of acute ocular inflammation, including vasodilation, miosis and hypotony.