{'fraction_non_alphanumeric': 0.015917602996254682, 'fraction_numerical': 0.0046816479400749065, 'mean_word_length': 5.03954802259887, '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}}
Biphasic effect of a kappa-opioid receptor agonist on plasma oxytocin levels in rats.

The effect of the kappa-opioid receptor agonist, bremazocine, on plasma oxytocin levels in rats was measured by a sensitive radioimmunoassay. Initially, a decrease in plasma oxytocin levels was seen 30 min after injection. This was in accordance with the bremazocine inhibition of oxytocin release after submaximal electrical stimulation seen in isolated neurointermediate lobes. The initial decrease in plasma oxytocin reversed, and 4 h after injection of bremazocine a 20-fold increase in the oxytocin level was seen. The rise in plasma oxytocin was paralleled by a rise in plasma sodium. The biphasic time course of the plasma oxytocin response can be explained by a combination of an inhibition of oxytocin release from the neurohypophysis and an increased water excretion leading to an elevation in plasma sodium, which may be responsible for the late rise in plasma oxytocin. Down-regulation of the opioid receptors may also contribute to the delayed rise in plasma oxytocin.