Fetal Neurohypophyseal Arginine Vasopressin and Arginine Vasotocin in Man and Sheep

Wr, Skowsky; Fisher, Derek J.

doi:10.1203/00006450-197705000-00001

Cited by 58 publications

(20 citation statements)

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“…In the human fetal pituitary, AVP has been identified as early as 11 wk of gestation (24,33). In other mammalian species, including the guinea pig, rabbit, sheep, and seal, the presence of AVP has been documented in the fetal pituitary gland during the last half of gestation (3,7,16,37).…”

Section: Discussionmentioning

confidence: 99%

The Dynamics of Vasopressin Release and Blood Volume Regulation During Fetal Hemorrhage in the Lamb Fetus

et al. 1979

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SummaryExperiments were performed on 11 long-term fetal lamb preparations (103-138 days of gestation) to investigate the sensitivity and relative responsiveness of the fetal volume receptors in modulating fetal plasma arginine vasopressin (pAVP) secretion and plasma renin activity (PRA) secretion during fetal hypovolemia and after fetal blood volume replacement. During fetal hemorrhage there were significant decreases (P < 0.05) in fetal hematocrit (34.7 f 2.58 to 27.0 f 1.64%), plasma proteins (3.14 f 0.15 to 2.78 f 0.19 g/100 ml), mean arterial blood pressure (MABP) (58.1 f 2.59 to 52.2 f 2.60 mmHg) and fetal arterial pH (7.38 f 0.01 to 7.35 f 0.01). A significant increase in fetal pAVP concentration from 0.73 f 0.21 to 34.9 f 10.04 pU/ml ( P < 0.01) and fetal PRA from 4.78 2.22 to 40.4 f 18.31 ng/ml/hr ( P < 0.05) was demonstrated at the peak of fetal hemorrhage. Two hr after correction of the fetoplacental blood volume, these values were back to base line levels. No change in either maternal pAVP or PRA was seen during fetal hemorrhage. When individual values for log pAVP and log PRA were plotted as a function of percent of fetoplacental blood volume removed the correlation coefficients were 0.82 and 0.60, respectively. A multiple regression analysis showed a high correlation of log pAVP and log PRA with the volume of blood removed and a low partial correlation with the fetal MABP. This suggests the decrease in fetal MABP was not the primary factor explaining the increase in pAVP and PRA during fetoplacental blood volume depletion. The data indicate that the fetal volume receptors for control of arginine vasopressin secretion are fullv functional in the last trimester of gestation and suggests that fetal pAVP and PRA are released as a; exponential function of the wrcent of feto~lacental blood volume de~letion. Finally, an isosmotic water shift from the fetal interstitial space to the fetal vascular space is described during fetal hemorrhage. SpeculationIt is suggested that a change in the equilibrium between the forces regulating fluid movement through the fetal capillary membranes, in accordance with Starling's principle, activates isosmotic water fluxes from the fetal interstitial space to the fetal vascular compartment counteracting the effects of fetal blood volume depletion. Therefore, the role of arginine vasopressin (AVP) release during fetal hemorrhage, if any, will be to act as a pressor substance helping to maintain fetal blood pressure. No major effect of AVP on placental membranes was demonstrated in vivo.Available information suggests that the newborn is capable of secreting vasopressin at birth and that both the osmoreceptors and volume control systems are fully functional (14,21,22).During fetal life, the increase in concentration of circulating vasopressin has been evoked by either osmolar or volume stimuli, using short-term fetal lamb preparations (exteriorized fetuses) (3, 32). However, the effects of surgical stress and anesthesia on the fetus may themselves have influenced this response (...

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Section: Discussionmentioning

confidence: 99%

The Dynamics of Vasopressin Release and Blood Volume Regulation During Fetal Hemorrhage in the Lamb Fetus

et al. 1979

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“…Changes in heart rate, cardiac output, and distribution of cardiac output to various fetal organs are similar to those seen during fetal hypoxia and suggest that vasopressin release may play an important role in the fetal cardiovascular response to stress. ORE Res 44: 430-436, 1979 ARGININE VASOPRESSIN has been detected in the neurohypophysis (Alexander et al, 1974a;Skowsky and Fisher, 1977; Vizsolyi and Perks, 1976a, b) and plasma (Rurak, 1975;Skowsky et al, 1974) of fetal sheep by midgestation. It is not known, however, whether arginine vasopressin has a role in normal fetal physiology or in the fetal response to stressful stimuli.…”

Section: Discussionmentioning

confidence: 99%

Hemodynamic responses of the sheep fetus to vasopressin infusion.

Iwamoto¹,

Rudolph²,

Keil³

et al. 1979

Circulation Research

142

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SUMMARYThe effects of intravenous infusion of vasopressin on the circulation of the fetus were studied in lambs in utero with chronically maintained intravascular catheters. Vasopressin infused in doses of 0.91-2.26 mU/min per kg fetal weight resulted in plasma levels of arginine vasopressin of 6.8-36.4 /iU/ml; these levels are similar to those achieved during fetal hypoxia. Petal mean arterial blood pressure increased from control levels of 47 ± 1.7 to 56 ± 1.9 nun Hg, and heart rate fell from 174 ± 4.1 to 144 ± 4.4 beats/min. Fetal cardiac output and its distribution and actual organ blood flows were measured before and during vasopressin infusion by the radionuclide-labeled microsphere technique. Combined ventricular output did not change significantly, but there was a redistribution of flow, with a marked reduction of the proportion of cardiac output to the gastrointestinal and peripheral circulations and an increase in the percent of cardiac output to the umbilical-placental, myocardial, and cerebral circulations. This redistribution was associated with a significant increase in fetal arterial Po» from 22 to 24 torr. Changes in heart rate, cardiac output, and distribution of cardiac output to various fetal organs are similar to those seen during fetal hypoxia and suggest that vasopressin release may play an important role in the fetal cardiovascular response to stress. ORE Res 44: 430-436, 1979 ARGININE VASOPRESSIN has been detected in the neurohypophysis (Alexander et al., 1974a;Skowsky and Fisher, 1977; Vizsolyi and Perks, 1976a, b) and plasma (Rurak, 1975;Skowsky et al., 1974) of fetal sheep by midgestation. It is not known, however, whether arginine vasopressin has a role in normal fetal physiology or in the fetal response to stressful stimuli. Plasma concentrations of arginine vasopressin in the sheep fetus have been shown to be elevated in response to various stimuli such as fetal hemorrhage, hypoxia, increased plasma sodium, and surgical manipulation (Alexander et al., 1974a, b;Rurak, 1975;Skowsky et al., 1973;Alexander et al., 1972).The cardiovascular system of the fetus responds to neurohypophysial hormones; intravenous infusion of arginine vasopressin into the sheep fetus has been shown to cause an increase in blood pressure and a decrease in heart rate (Rurak, 1975;Alexander et al., 1976). At present there is no information regarding the specific actions of arginine vasopressin on the cardiovascular system of the fetus. It is known that, in the adult, arginine vasopressin causes bradycardia and vasoconstriction of certain vascular beds, resulting in an increase in blood pressure (Vizsolyi and Perks, 1976a;Altura and Altura, 1977;Schmid et al., 1974). Our studies were undertaken to determine whether these responses are present in the fetus, and to characterize further the action of vasopressin on the hemodynamics of the sheep fetus. The nuclide-labeled microsphere method (Rudolph and Heymann, 1967;Heymann et al., 1977) was used to determine the distribution of combined ventricular output to v...

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“…Data regarding fetal vasopressin physiology, however, are meager. Vasopressin has been identified in the human fetal pituitary at 10-12 weeks of gestation (9,12) and in the fetal pituitary of other mammalian species, including the guinea pig, sheep, and seal, during the last half of gestation (1,2,10,12,14). In addition, in the sheep and monkey, significant concentrations of circulating vasopressin have been detectable in fetal blood during the last half of gestation (1, 1 l ) , and increases in circulating levels have been evoked either by osmolar or volume (hemorrhage) stimuli (1,11).…”

Section: Speculationmentioning

confidence: 99%

Arginine Vasopressin Response to an Osmotic Stimulus in the Fetal Sheep

et al. 1978

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Summary MATERIALS AND METHODSBaseline plasma osmolality (pOsm) and plasma arginiie vasopressin (pAVP) were measured in chronically catheterized fetal sheep. Mean baseline pAVP in fetuses from 101-120 days was 1.9 + 0.46 pU/ml (mean * SEM) with a pOsm of 293 rt 1.8 mOsm/kg. In fetuses of 121-141 days of gestation, mean pAVP was significantly lower, 0.77 0.19 pU/ml (P < 0.05), with a similar pOsm (293 2 1.9 mOsm/kg). The logarithmic baseline pAVP values were linearly correlated with pOsm for both groups. Hypertonic saline infusion resulted in a similar increase in the log pAVP corrected for the rise in pOsm in the 101-120-day fetuses and in 121-141-day fetuses. The slope of this response was similar to that of the steady state relationship. The data indicates that the fetal osmoreceptor system for control of arginine vasopressin secretion is fully functional in the last trimester of pregnancy. SpeculationThe fetal hypothalamic posterior pituitary system appears to show a relatively heightened response to increases in plasma osmolality during the last trimester of gestation. This may reflect the heightened hypothalamic activity postulated to explain the high circulating growth hormone levels at this time. The higher baseline plasma vasopressin levels in the younger fetuses would support this view. Alternatively, the augmented responsiveness may represent an adaptive response to the immaturity of the fetal kidney with respect to free water clearance or an adaptive response to some extrarenal function of the hormone on salt and water homeostasis in utero.Vasopressin secretion is regulated by two systems of r e c e p tors: the osmoreceptors located in or near the supraoptic nuclei in the hypothalamus and a series of volume receptors, including left atrial stretch receptors and carotid sinus and aortic arch baroreceptors. Available information suggests that the newborn is capable of secreting vasopressin at birth and that both the osmoreceptor and volume control systems are functional (3-6). Data regarding fetal vasopressin physiology, however, are meager. Vasopressin has been identified in the human fetal pituitary at 10-12 weeks of gestation (9, 12) and in the fetal pituitary of other mammalian species, including the guinea pig, sheep, and seal, during the last half of gestation (1,2,10,12,14). In addition, in the sheep and monkey, significant concentrations of circulating vasopressin have been detectable in fetal blood during the last half of gestation (1, 1 l ) , and increases in circulating levels have been evoked either by osmolar or volume (hemorrhage) stimuli (1, 11). However, little is known about the sensitivity and relative responsiveness of the fetal osmoreceptor control system. The present studies were designed to provide this information. 5Pregnant Columbia or Columbia-Suffolk ewes were obtained from a local source and the gestational age based on the induced ovulation technique (7). The animals were maintained in the vivarium and fasted 4 8 hr before surgery. The pregnant ewes were anesthetized using a m...

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Fetal Neurohypophyseal Arginine Vasopressin and Arginine Vasotocin in Man and Sheep

Cited by 58 publications

References 8 publications

The Dynamics of Vasopressin Release and Blood Volume Regulation During Fetal Hemorrhage in the Lamb Fetus

The Dynamics of Vasopressin Release and Blood Volume Regulation During Fetal Hemorrhage in the Lamb Fetus

Hemodynamic responses of the sheep fetus to vasopressin infusion.

Arginine Vasopressin Response to an Osmotic Stimulus in the Fetal Sheep

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