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The observation of plasma vasopressin elevations in rats which had been held manually for 1–2 min before decapitation prompted a study of this and other stressful stimuli. Plasma vasopressin concentrations determined by RIA [picograms per ml (±SEM)] were: 1) immediate decapitation after removal from cage, 1.69 ± 0.28; 2) manual restraint for 3 min, 42.4 ± 12.3; 3) light ether anesthesia, 1.97 ± 0.32; 4) forced exercise in the activity wheel (3 min), 2.09 ± 0.28; 5) swimming (3 min), 2.2 ± 0.44; 6) noise by continuous hammering on cages (3 min), 1.64 ± 0.37; 7) electric shock in plastic restrainers, 93 ± 35; 8) restraint in plastic restrainers without electric shock (control for group 7), 1.87 ± 0.43; and 9) body compression by firm squeeze around the trunk (1 min), 283 ± 111 (range, 30–1200 pg/ml). Aside from electric shock, which could well have caused direct excitation of neurohypophysis, no stressful stimulus produced vasopressin elevations except the light squeeze of manual restraint and the...

Previous studies have suggested that oxytocin may have an intragranular association with the posterior pituitary binding protein neurophysin I (NPI), and vasopressin with neurophysin II (NPII) in the ox. We have studied the possible relationship between oxytocin and NPI, and vasopressin and NPII at their presumed sites of synthesis in the bovine hypothalamus. Separate regions of the supraoptic (SON) and paraventrieular (PVN) nuclei from both sides of the hypothalamus and the posterior lobes of the pituitary glands (PL) of 4 steers were homogenized and extracted. The oxytocin and vasopressin content of these homogenates was determined by bioassay. Vasopressin was also measured by radioimmunoassay, as were NPI and NPII. Both hormones and both neurophysins were found in SON, PVN and PL. The concentrations of NPI and oxytocin in SON and PVN were the same. In the PVN the concentrations of oxytocin and vasopressin and those of NPI and NPII were similar. In the SON, however, NPII and vasopressin concentrations w...

The relative effects of 3 stimuli in the release of vasopressin (VP) by the fetus were examined in 19 chronically instrumented fetal lambs, 118-135 days gestational age. The fetus was exposed to: 1) 30-min administration of 10% O2 to the pregnant ewe, 2) 20 min of partial occlusion of the umbilical cord, or 3) 2 min of complete occlusion of the umbilical cord. Twelve studies were conducted for each of these experimental protocols. The rises (mean +/- SE) in plasma VP in the 3 groups were 29.9 +/- 8.9, 48.9 +/- 11.5, and 157.8 +/- 12.5 pg/ml, respectively; the corresponding falls in PaO2 were 9.2 +/- 0.7, 7.7 +/- 0.9, and 12.7 +/- 1.2 mm Hg. pHa did not change in the group receiving 10% O2, fell by 0.11 +/- 0.02 and 0.14 +/- 0.01 after partial and complete occlusion of the umbilical cord. The rises in mean arterial pressure were 6 +/- 2.2, 10 +/- 1.9, and 23 +/- 3.1 mm Hg, respectively, at the end of the 3 procedures. The rise in plasma osmolality ranged from 2-8 mosmol/kg in all 3 groups. Linear regression analyses showed that log VP was negatively correlated with PaO2 (r = -0.827; P less than 0.01) and pHa (r = -0.706; P less than 0.01) and positively correlated to mean arterial pressure (r = 0.607; P = 0.01), but was not significantly correlated to plasma osmolality. Our present findings suggest that hypoxemia and acidemia are associated with and may both be potent stimuli for VP release in the hypoxic fetus. Increased release together with decreased rate of metabolism by the placenta offer an explanation for the very high VP levels found in the neonate after labor and delivery.

The concentrations of vasopressin in the plasma and cerebrospinal fluid (CSF) of the chronically catheterized fetal lamb were measured under basal and hypoxic conditions. Under basal conditions, samples were obtained from 13 fetal lambs of 117-146 days gestation. The mean +/- SEM vasopressin level in CSF was 19.5 +/- 1.5 pg/ml; the mean plasma vasopressin level of 1.9 +/- 0.2 pg/ml was significantly less (P less than 0.001). No consistent change in concentrations of vasopressin in CSF was observed with gestational maturation in 3 animals sampled sequentially or in individual samples obtained over the last 32 days of gestation. The mean vasopressin concentration in the CSF of the pregnant ewe was 5.1 +/- 0.4 pg/ml. The gradients for osmolality, sodium, and potassium between fetal plasma and CSF were: osmolality, 298.4 +/- 1.6 to 304.3 +/- 1.4 mosmol/kg; sodium, 140.9 +/- 0.5-142.5 +/- 0.5 meq/liter; and potassium, 4.3 +/- 0.1 to 3.3 +/- 0.1 meq/liter. Fetal hypoxia was induced by exposure of the ewe to 10% O2 in N2 for 30 min. The concentration of vasopressin increased from 1.7 +/- 0.3 to 277 +/- 144 pg/ml (P less than 0.001) in fetal plasma and from 21.4 +/- 3.8 to 47.1 +/- 9.9 pg/ml (P less than 0.04) in fetal CSF. When the ewe was exposed to room air under comparable experimental conditions, no similar changes in plasma or CSF vasopressin levels were observed in the fetus. Infusion of vasopressin into the fetal jugular vein at 1.0 mU/min for 30 min increased plasma concentrations from 2.3 +/- 0.5 to 83 +/- 17 pg/ml, while the CSF vasopressin values were 31.9 +/- 5.9 (basally) and 30.7 +/- 4.8 pg/ml (after infusion). Mean plasma and CSF osmolality, sodium, and potassium were not changed by any of these experimental interventions. We conclude that 1) under basal conditions, high concentrations of vasopressin are present in the CSF of the fetal lamb, the blood-CSF barrier appears to be impermeable to vasopressin, and concentrations of the hormone in fetal plasma are less than those in CSF; and 2) hypoxia is a potent stimulus of vasopressin release in both fetal plasma and CSF. The route of vasopressin released into the fetal CSF may be distinct from that released into plasma.