Arginine vasopressin mediates cardiovascular responses to hypoxemia in fetal sheep

Abstract

Acute hypoxemia results in hypertension, bradycardia, and cardiac output redistribution in fetal sheep. The blood flow redistribution is produced by differential changes in vascular resistance of various fetal organs. alpha-Adrenergic activity is one of the few vasoconstrictor mechanisms thus far identified in the hypoxemic fetal sheep. Arginine vasopressin (AVP) is a potent vasoconstrictor in adults. Since AVP administration to the normoxic fetus mimics some of the fetal cardiovascular responses to hypoxemia and fetal plasma AVP levels increase with hypoxemia, we examined the hypothesis that AVP modifies the fetal cardiovascular response to hypoxemia by changing the vascular resistance of some fetal vascular beds. To test this we determined fetal systemic arterial pressure and fetal cardiac output and its distribution during hypoxemia with and without the V1 AVP antagonist d(CH2)5-Tyr(Me)AVP. Fourteen fetal sheep (0.79-0.90 of gestation) were chronically catheterized. Five days after surgery fetal hypoxemia was induced by introducing a mixture of 95% N2-5% CO2 (10-20 l/min) into a maternal tracheal catheter. The hypoxemia was maintained for 40 min. Fetal heart rate, systemic arterial blood pressure, and combined ventricular output and its distribution (radiolabeled microspheres) were measured before hypoxemia, at 20 min of hypoxemia alone, and at 20 min of hypoxemia plus either AVP antagonist (n = 5) or NaCl 0.9% (n = 5, controls). Fetal hypertension and bradycardia were partially reversed after the AVP antagonist administration during hypoxia.(ABSTRACT TRUNCATED AT 250 WORDS)

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.…”

Afferent and efferent components of the cardiovascular reflex responses to acute hypoxia in term fetal sheep.

“…The increase in femoral resistance in denervated fetuses during late hypoxia may be attributed to release of catecholamines as a direct result of hypoxia on the adrenal gland. Increased peripheral vasoconstriction in late hypoxia both in intact and denervated fetuses may also be attributed to increased release of vasoconstrictor humoral agents such as arginine vasopressin (Perez, Espinoza, Riquelme, Parer & Llanos, 1989) and angiotensin II (Iwamoto & Rudolph, 1981). Fetal survival In acute isocapnic hypoxia the fetus mounts physiological compensatory mechanisms which ensure a redistribution of the circulation to maintain an adequate perfusion to the cerebral, myocardial and adrenal circulations.…”

“…One plausible candidate may be arginine vasopressin (AVP) since its concentration in the fetal circulation increases during hypoxia (Rurak, 1978;Daniel, Stark, Zubrow, Fox, Husain & James, 1983;Iwamoto et al 1983;Picquadio, Brace & Cheung, 1990; Raff, Kane & Wood, 1991). AVP infusion in normoxaemic fetal sheep 445 D. A. GIUSSANI AND OTHERS produces a vasoconstriction in the carcass but no significant change in other organs , and administration of a V1 antagonist reverses the rise in systemic arterial pressure observed during hypoxia (Perez et al 1989 mimic the naturally occurring rise in plasma AVP concentration during hypoxia, permits them to survive acute hypoxia even after combined carotid chemodenervation and a-adrenergic blockade (Giussani, Spencer, Moore, Bennet & Hanson, 1992). Alternative candidates may be renin/angiotensin and neuropeptide Y.…”

Fetal endocrine responses to prolonged reduced uterine blood flow are altered following bilateral sectioning of the carotid sinus and vagus nerves

“…AVP administration to normoxic fetuses leads to cardiovascular changes similar to those observed with acute hypoxia including a transient bradycardia and hypertension (Rurak 1978, Iwamoto et al 1979, Tomita et al 1985. Furthermore, fetal plasma AVP concentrations increase with the onset of acute hypoxia (Rurak 1978, Daniel et al 1983, Raff et al 1991, and administration of a V 1 receptor antagonist partially reverses the associated cardiovascular responses (Perez et al 1989). The role of the peripheral chemoreceptors in mediating the AVP response to acute hypoxia remains controversial.…”