{'fraction_non_alphanumeric': 0.031049250535331904, 'fraction_numerical': 0.026231263383297645, 'mean_word_length': 4.75076923076923, '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}}
Vasodilation induced by a specific vasopressin V2 agonist in dogs

Vasopressin V2 agonists increase cardiac output and lower total peripheral resistance within minutes when infused into conscious dogs. The purpose of this study was to determine the mechanisms of these haemodynamic effects. Two groups of dogs were studied. In the first group, six dogs were instrumented for the measurement of mean arterial pressure and cardiac output (electromagnetic flowmeter) at least 1 week before the experiment. They were then anaesthetized with pentobarbital and the central nervous system was destroyed. Mean arterial pressure was maintained with an infusion of noradrenaline. After it had remained stable for 30 min the dogs received an intravenous infusion of 4-valine-8-D-arginine vasopressin (VDAVP), a specific V2 agonist, 10 ng/kg per min. Mean ± s.e.m. arterial pressure fell from 97.6 ± 1.8 to 69.1 ± 2.5 mmHg, but cardiac output did not change significantly. Total peripheral resistance fell from 1322.5 ± 151 to 859.7 ± 84.9 units. Thus, VDAVP exerts haemodynamic effects in the absence of the central nervous system and appears to act primarily as a vasodilator. A second group of six anaesthetized dogs was studied in which femoral blood flow was measured with an electromagnetic flow probe during intravenous and intrafemoral arterial infusion of VDAVP, 10 ng/kg per min. Blood flow increased by 27.9 ± 5.4 ml/min from a control value of 65.1 ± 12.6 ml/min with intra-arterial infusion of VDAVP, but did not change significantly with intravenous infusion. Mean arterial pressure remained unchanged under both conditions. These results suggest that VDAVP lowered femoral resistance through a peripheral action, either directly or by releasing an endogenous vasoactive substance, indicating the presence of V2-like receptors in the femoral vascular bed of the dog.