Hemodynamic effects of arginine vasopressin in rats adapted to chronic hypoxia

Abstract

Acute and chronic pulmonary and systemic hemodynamic responses to arginine vasopressin (AVP) were examined in 4-wk hypoxia-adapted and air control rats. AVP, administered intravenously as bolus injections or sustained infusions, produced major dose-dependent V1-receptor-mediated reductions in mean pulmonary arterial pressure in hypoxia-adapted rats. These effects were comparable in pentobarbital-anesthetized, thoracotomized animals and in conscious, intact rats. Chronic infusions of AVP induced a sustained reduction in mean pulmonary arterial pressure and partially prevented the development of pulmonary hypertension without changing systemic arterial pressure. AVP induced significant decreases in cardiac output in both groups; the cardiac output response was not significantly different in hypoxia-adapted and air control animals. AVP induced almost no change in MPAP in air control rats. Furthermore the systemic pressor effects of AVP were significantly blunted in hypoxia-adapted rats compared with air controls. We conclude that the pulmonary depressor and blunted systemic pressor effects of AVP observed in hypoxia-adapted rats may be related to release of a vasodilator, such as endothelium-derived relaxing factor, vasodilator prostaglandins, or atrial natriuretic peptides. Further study is needed to elucidate these mechanisms and assess the usefulness of AVP and/or its analogues in the treatment and prevention of hypoxia-induced pulmonary hypertension.

Systemic vasoconstriction modulates the responses of pulmonary vasculature and airway to vasoconstrictors in anesthetized rats

“…This finding is consistent with the previous observations that vasopressin caused neither vasodilation nor vasoconstriction, when pulmonary vessels were not precontracted [26,27]. In contrast, rat pulmonary arteries or perfused rat lungs, which were precontracted by U46619 or hypoxia, exhibited vasodilation in response to vasopressin [26,27,[28][29][30].…”

Copeptin and risk stratification in patients with acute dyspnea

“…Second, vasopressin has been shown to have vasoconstrictive effects, which may correlate to the hypoxia induced-vasoconstriction in severe chronic obstructive pulmonary disease [32,33]. Increased concentrations of vasopressin may compensate for vasopressin (V1) receptor down-regulation following exposure to sustained hypoxemia [34]. Third, Copeptin is significantly increased in bacterial infection and febrile conditions [13,35].…”

C-reactive protein and copeptin: prognostic predictors in chronic obstructive pulmonary disease exacerbations

“…Possible explanations for elevation of copeptin levels in patients with COPD exacerbation could be related to vasoconstriction [34][35][36] and downregulation of the V1-receptor [37] due to sustained hypoxemia. Furthermore, endotoxin stimulates release of vasopressin.…”