{'fraction_non_alphanumeric': 0.02780191138140747, 'fraction_numerical': 0.0, 'mean_word_length': 5.816568047337278, '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}}
Modulation of vascular smooth muscle contraction by the endothelium.

The vascular endothelium is the layer of squamous epithelial cells that is in direct contact with the blood. In addition to its other important functions, which include capillary transport, regulation of plasma lipids, and participation in the control of hemostasis, it modulates the reactivity of vascular smooth muscle. This regulatory role is accomplished through several mechanisms: The layer (a) interposes a physical barrier between the vascular smooth muscle and hormones and other vasoactive substances circulating in blood; (b) it extracts or metaboli­ cally degrades vasoactive substances such as norepinephrine, serotonin, and kinins and thereby prevents or diminishes their activity in vascular smooth muscle; (c) it converts precursors (e.g. angiotensin I) into vasoactive products; (d) it secretes known vasoactive substances, primarily prostacyclin; and (e) it releases other still unidentified inhibitory and excitatory mediators in response to vasoactive stimuli. This review will summarize the evidence that the latter mechanism exists in mammalian blood vessels.