{'fraction_non_alphanumeric': 0.01595358955765047, 'fraction_numerical': 0.0, 'mean_word_length': 5.571428571428571, '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}}
Mechanism of hyperosmolarity inhibition of vascular contractility.

Studies were made of the responses of the vascular bed of cat hind leg to intraarterial injection of noradrenaline, angiotensine, tyramine and vasopressine, as well as of carotid occlusion upon increasing the tissue osmolarity through intraarterial hypertonic infusion. The limb was perfused at constant blood flow. Hyperosmolarity inhibited the contractile effects of all stimuli studied. The inhibition of the contractility was greater in the case of tyramine and identical in the case of the remaining vasoconstrictor agents. Increased KCl content or the addition of L-ascorbic acid to the hypertonic solution with preservation of the same hyperosmolarity reduced the inhibition of the contractile responses to noradrenaline and angiotensine. The restoration of the contractility was much more pronounced upon simultaneous increase in the KCl content and addition of L-ascorbic acid. No recovery of the contractile effect of tyramine was observed. The mechanism of hyperosmolarity inhibition of the vascular contraction is discussed. In all vasoconstrictor stimuli the inhibition is connected primarily with disruption of the transmembrane exchange of Na+ and Ka+. In some vasoconstrictor agents, e. g. tyramine, there is disturbance in the specific mechanism connected secondarily with vascular contraction.