{'fraction_non_alphanumeric': 0.03355704697986577, 'fraction_numerical': 0.027361899845121322, 'mean_word_length': 6.072992700729927, '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}}
Vascular serotonin receptors and blood pressure regulation

In most vascular beds, receptors mediating contraction to serotonin are of the 5HT2 type (defined by [3H]‐spiperone binding in brain tissue). Research on vascular serotonin receptors has been prompted by the development of ketanserin, a potent 5HT2‐receptor antagonist. Recent data suggest that ketanserin also possesses α‐receptor antagonist activity and that this property accounts for its antihypertensive activity in spontaneously hypertensive rats (SHR). The multiple blocking activities of ketanserin have prompted a search for more selective 5HT2‐receptor antagonists to elucidate the role of vascular serotonin receptors in blood pressure regulation. Consequently, 1‐(1‐naphthyl)piperazine (1‐NP) and LY53857, an ergoline derivative, have been identified as potent and highly selective 5HT2‐receptor antagonists in vascular tissue. 1‐(1‐napthyl)piperazine and LY53857 show approximately 2,000‐ and 300,000‐fold greater affinity, respectively, for 5HT2‐receptors than for α‐receptors compared to a 60‐fold selectivity of ketanserin. However, neither 1‐NP nor LY53857 lowered blood pressure in the SHR in doses that markedly shifted the pressor response to serotonin but did not antagonize α‐adrenergic receptors. Furthermore, blood pressure reduction in the SHR correlated poorly with the ability of several “5HT2‐receptor antagonists” to bind to 5HT2‐receptors and correlated extremely well with the binding of these agents to α‐receptors. Thus, in SHR, 1) antihypertensive activity of ketanserin occurred in doses that block α‐receptors and not at lower doses that block serotonin receptors, 2) more specific serotonin antagonists that did not block α‐receptors in vivo did not lower blood pressure, and 3) the reduction in blood pressure produced by a series of serotonin receptor antagonists correlated with their ability to block α‐receptors but not 5HT2‐receptors.