Plasma vasopressin levels during hypoxaemia and the cardiovascular effects of exogenous vasopressin in foetal and adult sheep.

Abstract

SUMMARY1. Foetal plasma vasopressin levels were measured by bio-assay in chronically catheterized sheep from 110 to 145 days gestation.2. In foetuses in good condition resting circulating vasopressin concentrations were generally undetectable ( < 5 Itu./ml.). In 15 % of the samples low concentrations (5-10 uu./ml.) were observed.3. Hypoxaemia in the foetus was caused by allowing the ewe to breathe 9 % 02-3 % CO2 in N2 for 1 hr. Plasma vasopressin levels rose in the foetus to 119 + 32 /zu./ml., whereas the hormone levels in the ewe were not routinely increased. In the foetus, the rise in plasma vasopressin levels was significantly related to the fall in pH and Pa ,0 during the hypoxia. 4. In foetuses in which the cervical vagosympathetic trunks were cut, the rise in plasma vasopressin levels (to 48 + 25 ,uu./ml.) during hypoxaemia was less than in intact foetuses. The increase was related only to the fall in arterial pH and the regression coefficient was less than in intact foetuses.5. During hypoxaemia arterial pressure rose and heart rate fell in the normal foetuses. The rise in arterial pressure was greatest when the plasma vasopressin concentration was highest.6. Spontaneous episodes of hypoxaemia (Paw,, < 15 mmHg) and/or acidaemia (pH < 7.30) occurred in four intact foetuses and four foetuses in which the cervical vagosympathetic trunks were cut; all of the latter lambs died in utero. Plasma vasopressin levels were elevated and the concentrations were inversely related to arterial pH.7. Intravenous infusions of vasopressin to foetuses increased plasma vasopressin levels to 6-202 #su./ml.; the rate of clearance of the hormone was three times that in adult ewes. There was a large increase in arterial pressure and bradyeardia. The hypertensive effects of vasopressin were relatively much greater in the foetus than in adult ewes.

Gestational age-dependent changes in the levels of mRNAs encoding cortisol biosynthetic enzymes and IGF-II in the adrenal gland of fetal sheep during prolonged hypoxemia

“…In response to short-term (60 min) hypoxemia, there are increases in fetal plasma concentrations of adrenocorticotrophin (ACTH), vasopressin and cortisol (Boddy et al 1974, Rurak 1978, Stark et al 1982, Akagi & Challis 1990. The magnitude of these changes varies at different gestational ages in relation to the progressive maturation of fetal HPA function.…”

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.…”

“…The role of the peripheral chemoreceptors in mediating the AVP response to acute hypoxia remains controversial. Bilateral sectioning of the cervical vagosympathetic trunk attenuates the response (Rurak 1978), whereas sinoaortic (Raff et al 1991) or carotid sinus (Giussani et al 1994) denervation does not. During prolonged RUBF, fetal plasma AVP concentrations increase to maximum values at 2 h and return to normoxic values after 12 h (Hooper et al 1990), suggesting a transient role in modulating fetal cardiovascular responses.…”

“…The role of the peripheral chemoreceptors in mediating these responses remains controversial. Sectioning of the cervical vagosympathetic trunk attenuates the rise in plasma AVP concentrations (Rurak 1978) whereas sinoaortic (Raff et al 1991) or carotid sinus denervation (Giussani et al 1994) does not. Furthermore, sinoaortic denervation attenuates the rise in plasma angiotensin II concentrations (Wood et al 1990) whereas carotid sinus denervation does not (Green et al 1997).…”

“…Under conditions of acute hypoxia in sheep, fetal plasma arginine vasopressin (AVP) (Rurak 1978, Daniel et al 1983, angiotensin II (Broughton Pipkin et al 1974) and catecholamine ( Jones & Robinson 1975, Gu et al 1985 concentrations increase. The role of the peripheral chemoreceptors in mediating these responses remains controversial.…”