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

Rurak, D. W.

doi:10.1113/jphysiol.1978.sp012275

Cited by 162 publications

(92 citation statements)

References 26 publications

(27 reference statements)

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“…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.…”

Section: Introductionmentioning

confidence: 99%

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

Braems

Han²,

Challis³

1998

Journal of Endocrinology

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Hypoxemia represents a major stress for the fetus, and is associated with alterations and adaptations in cardiovascular, metabolic and endocrine responses, which in turn may affect tissue growth and differentiation. To determine the effects of hypoxemia on fetal adrenal activity and growth, we subjected sheep fetuses at days 126-130 and 134-136 (term 145 days) to reduced PaO 2 by reducing the maternal fraction of oxygen for 48 h (mean reduction of 6·8 mmHg), without change in arterial pH or PaCO 2 . This stimulus resulted in similar increases in the plasma immunoreactive ACTH response at both ages. Among adrenal steroids, plasma cortisol (C21 4 ) rose in both groups of animals, but plasma androstenedione (C19 4 ) declined marginally, resulting in a pronounced increase in the cortisol:androstenedione ratio in the plasma that was greater and more sustained in the older fetuses. In the younger fetuses, after 48 h of hypoxemia, there were no significant changes in mRNAs encoding steroidogenic enzymes in the fetal adrenal gland. However, in the older fetuses, hypoxemia resulted in significantly increased levels of mRNAs encoding P450 scc , P450 C21 and 3 -hydroxysteroid dehydrogenase, but not for P450 C17 , in the fetal adrenal gland. Levels of IGF-II mRNA in the fetal adrenal gland fell in both groups of fetuses, and this response was greater at the later gestational age. We conclude that sustained hypoxemia is a potent stimulus which activates adrenal steroidogenesis in the late gestation fetal sheep. The resultant increase in cortisol synthesis is associated with decreased expression of adrenal IGF-II mRNA. We speculate that this relationship might influence patterns of fetal organ growth and differentiative function in response to fetal stress such as hypoxemia.

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Section: Introductionmentioning

confidence: 99%

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

Braems

Han²,

Challis³

1998

Journal of Endocrinology

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“…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.…”

Section: Discussionmentioning

confidence: 96%

“…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.…”

Section: Discussionmentioning

confidence: 99%

“…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).…”

Section: Introductionmentioning

confidence: 99%

“…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.…”

Section: Introductionmentioning

confidence: 99%

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

Stein

White²,

Homan³

et al. 1998

Journal of Endocrinology

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The present study examines the effect of carotid sinus/ vagosympathetic denervation on fetal endocrine responses to prolonged reduced uterine blood flow (RUBF). Fetal sheep had vascular catheters inserted following bilateral sectioning of the carotid sinus and vagus nerves (denervated, n=7) or sham denervation (intact, n=7). Uterine blood flow was mechanically restricted at 126·1 0·7 days (mean ...) for 24 h, decreasing arterial oxygen saturation by 47·3 2·6% (P<0·01). Fetal plasma samples were obtained at 1, 3, 6, 12 and 24 h for subsequent analyses of arginine vasopressin (AVP), angiotensin II and catecholamines. The AVP response to prolonged RUBF was markedly attenuated in denervated fetuses (15·6 3·6 to 34·9 6·0 pg/ml) when compared with intact (10·0 1·4 to 127·3 28·4 pg/ml). In contrast, intact fetuses demonstrated no change in plasma angiotensin II concentrations with RUBF whereas denervated fetuses demonstrated a marked increase from 47·5 18·9 to 128·7 34·2 pg/ml. The norepinephrine and epinephrine responses to prolonged RUBF were attenuated in denervated fetuses (950·1 308·9 and 155·8 58·5 to 1268·3 474·6 and 290·6 160·2 pg/ml respectively) when compared with intact (1558·3 384·4 and 547·3 304·7 pg/ml to 3289·2 1219·8 and 896·8 467·8 pg/ml respectively). These results support a role for the peripheral chemoreceptors in mediating fetal endocrine responses to prolonged RUBF, which may in part lead to the altered cardiovascular responses observed in denervated fetuses under these conditions.

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Mechanism of arginine vasopressin suppression of ovine fetal lung fluid secretion: Lack of V2-receptor effect

Albuquerque

Nijland

Ross

1998

J. Matern. Fetal Med.

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Fetal lung liquid production is essential for in utero pulmonary development, and the resorption of lung liquid at birth facilitates neonatal transition. Lung liquid also contributes importantly to amniotic fluid volume. Factors that influence lung liquid production/resorption may, therefore, impact fetal pulmonary growth and development as well as amniotic fluid homeostasis. Arginine vasopressin (AVP) inhibits fetal lung liquid production and facilitates lung liquid resorption. In view of studies administering fetal AVP or the V2 receptor agonist, 1 desamino 8‐D AVP (dDAVP) for the regulation of amniotic fluid volume, we sought to determine the impact of AVP V2 receptor stimulation on fetal lung liquid production. Eight near‐term ovine fetuses (130 ± 2 d; term = 145 d) were prepared with hind limb vascular catheters, a bladder catheter, and a tracheal catheter. Each ewe received vascular and amniotic catheters. After 5 days of recovery, the animals were studied for a 2‐hr control period and for 2 hr following intravenous dDAVP injection (1 ng/kg). Lung liquid and urine flow rates and plasma electrolyte and osmolality composition were determined at 30‐min intervals. To confirm fetal lung liquid suppression in response to AVP, two animals received an intravenous injection of AVP (2 ng/kg) 24 hr after the first experiment. dDAVP administration had no effect on lung liquid production (3.4 ± 0.4 ml/kg/h), electrolyte concentrations, or osmolality. Fetal urine electrolyte concentrations and osmolality (154 ± 24–295 ± 22 mOsm/kg H2O) increased in response to dDAVP, whereas urine flow decreased (9.4 ± 2.5–4.2 ± 1.5 ml/kg/h). In the fetuses exposed to AVP, lung liquid production decreased (3.3–1.6 ml/kg/h). As AVP, although not dDAVP, inhibited fetal lung liquid production, these results indicate that AVP effects on lung liquid are likely mediated via the AVP V1 receptor, not the V2 receptor. The use of fetal administration of dDAVP for the regulation of urine production and amniotic fluid volume will not adversely impact lung liquid production. J. Matern.–Fetal Med. 7:177–182, 1998. © 1998 Wiley‐Liss, Inc.

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

Cited by 162 publications

References 26 publications

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

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

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

Mechanism of arginine vasopressin suppression of ovine fetal lung fluid secretion: Lack of V2-receptor effect

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