{'fraction_non_alphanumeric': 0.04933586337760911, 'fraction_numerical': 0.04364326375711575, 'mean_word_length': 4.994318181818182, 'pattern_counts': {'":': 0, '<': 3, '<?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}}
Inhibition of Aggregation and Calcium Influx of Human Platelets by Nitrendipine

Since platelet aggregation is associated with an increase in intracellular calcium concentration, the effects of the calcium entry blocker nitrendipine on 45Ca2+ influx and on aggregation of human platelets were studied. The thrombin-induced 45Ca2+ influx (60 pmol/ 10−5 platelets, p < 0.01 vs. basal influx) was reduced by nitrendipine (4 × 10−5 M) to 20 pmol/108 platelets. Oral intake of 2 × 20mg/day of nitrendipine by normotensive volunteers (n = 12) reduced ADP (1.0 μM)-induced platelet aggregation. ex vivo (p < 0.05). Adrenaline-induced aggregation was inhibited (p < 0.05) at low concentrations of adrenaline (0.1 μM) at rest and also at higher concentrations (1 μM) after 5 min of exercice (150 W), while exercise itself had no measurable effect on platelet aggregation. The results demonstrate that nitrendipine, by inhibiting 45Ca2+ influx and aggregation of human platelets, potentially exerts additional warranted effects apart from blood pressure reduction.