Osmotic threshold and sensitivity for vasopressin release and fos expression by hypertonic NaCl in ovine fetus

In adults, hyperosmolality stimulates central osmoreceptors, resulting in arginine vasopressin (AVP) secretion. Near-term fetal sheep have also developed mechanisms to respond to intravascular hypertonicity with stimulation of in utero AVP release. However, prior studies demonstrating fetal AVP secretion have utilized plasma tonicity changes greater than those required for adult osmotically induced AVP stimulation. We sought to examine near-term fetal plasma osmolality threshold and sensitivity for stimulation of AVP secretion and to correlate plasma hormone levels with central neuronal responsiveness. Chronically instrumented ovine fetuses (130 +/- 2 days) and maternal ewes simultaneously received either isotonic or hypertonic intravascular NaCl infusions. Maternal and fetal plasma AVP and angiotensin II (ANG II) levels were examined at progressively increasing levels of plasma hypertonicity. Intravenous hypertonic NaCl gradually elevated plasma osmolality and sodium levels. Both maternal and fetal plasma AVP increased during hypertonicity, whereas ANG II levels were not changed. Maternal AVP levels significantly increased with a 3% increase in plasma osmolality, whereas fetal plasma AVP significantly increased only at higher plasma osmolality levels (over 6%). Thus the slope of the regression of AVP vs. osmolality was greater for ewes than for fetuses (0.232 vs. 0.064), despite similar maternal and fetal plasma osmolality thresholds for AVP secretion (302 vs. 304 mosmol/kg). Hyperosmolality induced Fos immunoreactivity (FOS-ir) in the circumventricular organs of the fetal brain. FOS-ir was also demonstrated in the fetal supraoptic and paraventricular nuclei (SON and PVN), and double labeling demonstrated that AVP-containing neurons in the SON and PVN expressed Fos in response to intravenous NaCl. These results demonstrate that, in the ovine fetus at 130 days of gestation, neuroendocrine responses to cellular dehydration are functional, although they evidence a relatively reduced sensitivity for AVP secretion compared with the adult.     

Plasma concentration of antidiuretic hormone in patients with chronic renal insufficiency on maintenance dialysis.

Radioimmunoassay of plasma arginine-vasopressin (AVP) in regularly dialyzed patients with chronic renal insufficiency revealed a parallel increase of AVP and plasma osmolality (POsm) before dialysis (4.16 +/- 0.36 pg/ml and 312.6 +/- 1.80 mOsm/1) and their parallel declin to the normal range (1.93 +/- 0.27 pg/ml and 292.0 +/- 1.27 mOsm/1) during dialysis. Plasma AVP correlated with POsm before and after dialysis (r = 0.611 and 0.453, p less than 0.01 and less than 0.05 respectively). The increase of AVP before dialysis was lower than would correspond to the rise of POsm and lower than that recorded in healthy subjects during dehydration. Statistical correlation between plasma AVP and indicators of body fluid volume changes between or during dialysis were not proved. We found statistical correlation between the mean blood pressure and AVP before dialysis (r = 0.468, p less than 0.05). These findings suggest that in chronic renal insufficiency changes of POsm remain primary regulating factor of AVP secretion. The expansion of extracellular fluid volume has probably only a modifying effect. It remains to be elucidated whether the revealed statistical relationship between the mean blood pressure and AVP before dialysis plays also a pathogenetic role in the development of hypertension in chronic renal insufficiency.     

Maternal DDAVP-induced hyponatremia preserves fetal urine flow during acute fetal hemorrhage

Maternal administration of DDAVP induces maternal and fetal plasma hyponatremia, accentuates fetal urine flow, and increases amniotic fluid volume. Fetal hemorrhage represents an acute stress that results in fetal AVP secretion and reduced urine flow rate. In view of the potential therapeutic use of DDAVP for pregnancies with reduced amniotic fluid volume, we sought to examine the impact of maternal hypotonicity during acute fetal hemorrhage. Chronically catheterized pregnant ewes (130 +/- 2 days) were allocated to control or to DDAVP-induced hyponatremia groups. In the latter group, tap water (2,000 ml) was administered intragastrically to the ewe followed by DDAVP (20 microg bolus, 4 microg/h) and a maintenance intravenous infusion of 5% dextrose water for 4 h to achieve maternal hyponatremia of 10-12 meq/l. Thereafter, ovine fetuses from both groups were continuously hemorrhaged to 30% of estimated blood volume over a 60-min period. DDAVP caused similar degree of reductions in plasma sodium and osmolality in pregnant ewes and their fetuses. In response to hemorrhage, DDAVP fetuses showed greater reduction in hematocrit than control fetuses (14 vs. 10%). Both groups of fetuses demonstrated similar increases in plasma AVP concentration. However, the AVP-hemorrhage threshold was greater in DDAVP fetuses (22.5%) than in control (17.5%). Hemorrhage had no significant impact on plasma osmolality, electrolyte levels, or cardiovascular responses in either group of fetuses. Despite similar increases in plasma AVP, DDAVP fetuses preserved fetal urine flow rates, with values threefold those of control fetuses. These results suggest that under conditions of acute fetal stress of hemorrhage, maternal DDAVP may preserve fetal urine flow and amniotic fluid volume.     

Prolonged prenatal hypernatremia alters neuroendocrine and electrolyte homeostasis in neonatal sheep

Arginine vasopressin (AVP) is a neuroendocrine hormone synthesized in the hypothalamus, and is stored and secreted by the posterior pituitary gland in response to stimuli such as plasma hypertonicity and hypotension. The primary physiologic roles of AVP include plasma osmolality and blood pressure regulation. We have previously demonstrated that chronic prenatal plasma hypertonicity alters the AVP regulatory pathway in newborn lambs. The objectives of the present study were to evaluate prolonged effects of antenatal plasma hypertonicity on neonatal plasma osmoregulation. Pregnant ewes at 119 +/- 3 days of gestation were water restricted to achieve and maintain hypertonicity until normal-term delivery. After delivery, ewes were provided food and water ad libitum and lambs were allowed maternal nursing. At the age of 28 days, blood samples were obtained for the analysis of plasma osmolality, electrolytes, and AVP levels from study (n= 5) and age-matched control (n= 6) lambs. Subsequently, lambs were euthanized, and the pituitary and hypothalamus were processed for the determination of pituitary AVP content by radioimmunoassay, and AVP gene expression by Northern analysis. In response to water restriction, maternal plasma osmolality significantly increased (306 +/- 1.1 to 326 +/- 1.2 mOsm/kg, P< 0.001). At the age of 28 days, plasma sodium level was higher in study (prenatally dehydrated) than control lambs (144.6 +/- 0.4 vs 142.6 +/- 0.3,P< 0.05). Study lambs had higher plasma AVP concentrations than the control lambs (4.1 +/- 0.4 vs 1.7 +/- 0.4 pg/ml,P< 0.05). Similarly, total pituitary AVP content was higher in thein utero hypertonic lambs than in the control lambs (6.5 +/- 1.0 vs 2.8 +/-1.2 microg, P< 0.05). However, there was no difference in hypothalamic AVP mRNA levels between the two groups. The present study demonstrates that chronic maternal and fetal plasma hypertonicity has prolonged effects on pituitary and plasma AVP, as well as plasma sodium in neonatal lambs, providing further evidence suggesting prenatal imprinting of osmoregulation through at least 1 month of age.     

Osmotic regulation of prolactin secretion in the fetal sheep

The functions of prolactin in the fetus remain speculative. No obvious physiological role has been found for the prolactin present in the fetal or maternal plasma and amniotic fluid compartments. The aim of the present study was to investigate changes in fetal plasma prolactin following intracerebroventricular (i.c.r.) administration to the fetus of artificial cerebrospinal fluid of different tonicities. A lateral ventricle catheter was placed in 11 fetuses at 107-128 days of gestation. Either isotonic artificial cerebrospinal fluid (300 mOsm.1(-1);n = 9), 15% polyethylene glycol (340 mOsm.1(-1);n = 5), or 7% distilled water in isotonic artificial cerebrospinal fluid (270 mOsm.1(-1);n = 9) was infused i.c.v. at 35 mu1.min-1 for 240 min. At 180 min thyrotropin releasing hormone (TRH) was administered through a fetal a fetal jugular catheter. Fetal carotid arterial blood gases, plasma osmolality and concentrations of prolactin, vasopressin (AVP), and norepinephrine (NE) were measured. Administration of hypotonic artificial cerebrospinal fluid produced an increase in fetal plasma prolactin from 46.6 +/- 36 ng.ml-1 at 0 min to 83.3 +/- 49 ng.ml-1 at 180 min (mean +/- SEM; P less than 0.05). No changes in either AVP or NE were observed. Administration of hypertonic artificial cerebrospinal fluid produced a decrease in plasma prolactin from 85 +/- 57 at time 0 to 49 +/- 35 at 180 min (P less than 0.05). No changes in either AVP or NE were observed. Fetal plasma prolactin, AVP, and NE did not change during control infusion of isotonic artificial cerebrospinal fluid.(ABSTRACT TRUNCATED AT 250 WORDS)     

Radioimmunoassay of arginine vasopressin in the plasma and urine.

We introduced the radioimmunoassay (RIA) of arginine vasopressin (AVP) with standard AVP and antiserum to AVP (both Calibiochem). The sensitivity of the system was increased from the declared 4pg to 1 pg per tube by preparing AVP-125I of high specific activity (about 1,500 mCi/mg) and by modifying the reaction conditions. The sensitivity of the method was adequate for measuring AVP in urine and in concentrated plasma extracts, even under physiological conditions. Reliability of the results depended upon maintenance of approximately the same osmolarity in all the RIA samples. The mean plasma AVP level, uncorrected for AVP extraction losses, was 1.52 +/- 0.20 pg/ml for an ad libitum fluid intake; in fluid deprivation it rose in proportion to the osmolarity of the plasma to 5.83 +/- 0.42 pg/ml at 12 hours and to 19.09 +/- 4.51 pg/ml at 36 hours. Extraction recovery of added AVP was about 63%. The urinary AVP concentration varied according to the patients' state of hydratation from undetectable values at UOsm less than 200 mOsm/1 to a mean 16.5 +/- 7.9 pg/ml in the presence of an ad libitum fluid intake and to 29.1 +/- 7.5 pg/ml after 12 hours' and 117.2 +/- 13.7 pg/ml after 36 hours' deprivation of fluids.     

A case of hyponatremia in panhypopituitarism caused by the primary empty sella syndrome

A 64-year-old woman was admitted for evaluation of hyponatremia. She was maintained on hypertonic saline administration. Without this therapy, the serum Na concentration decreased progressively to 127 mEq/L and the plasma osmolality to 254 mOsm/Kg H2O, on Day 3. At that time, the concentration of antidiuretic hormone (ADH) was as high as 3.5 pg/ml. A skull radiogram revealed an enlarged sella turcica. Computed tomography (CT) revealed a low density in the sella, and magnetic resonance imaging revealed equal intensity of the sella turcica and the cerebrospinal fluid. A diagnosis of empty sella syndrome was made by metrizamide cisternography in conjunction with CT scanning. A diagnosis of panhypopituitarism was made by endocrine function tests. 123I-thyroidal uptake was 6% when her serum TSH was 10.9 microU/ml, suggesting that she might also have primary hypothyroidism. When this patient was given glucocorticoid before levothyroxine replacement, her serum Na concentration rose up to about 140 mEq/L and a normal relationship between her plasma ADH level (2.4 pg/ml) and plasma osmolality (281 mOsm/kg H2O) was restored. Therefore, it was suggested that ADH hypersecretion induced by the glucocorticoid deficiency might in part contribute to the development of hyponatremia. This is the case of primary empty syndrome associated with panhypopituitarism, in whom initial symptom was caused by hyponatremia.     

Sex differences in osmotic regulation of AVP and renal sodium handling.

To determine sex differences in osmoregulation of arginine vasopressin (AVP) and body water, we studied eight men (24 +/- 1 yr) and eight women (29 +/- 2 yr) during 3% NaCl infusion [hypertonic saline infusion (HSI); 120 min, 0.1 ml. kg body wt(-1). min(-1)]. Subjects then drank 15 ml/kg body wt over 30 min followed by 60 min of rest. Women were studied in the early follicular (F; 16.1 +/- 2.8 pg/ml plasma 17beta-estradiol and 0.6 +/- 0.1 ng/ml plasma progesterone) and midluteal (L; 80.6 +/- 11.4 pg/ml plasma 17beta-estradiol and 12.7 +/- 0.7 ng/ml plasma progesterone) menstrual phases. Basal plasma osmolality was higher in F (286 +/- 1 mosmol/kgH(2)O) and in men (289 +/- 1 mosmol/kgH(2)O) compared with L (280 +/- 1 mosmol/kgH(2)O, P < 0.05). Neither menstrual phase nor gender affected basal plasma AVP concentration (P([AVP]); 1.7 +/- 4, 1.9 +/- 0.4, and 2.2 +/- 0.5 pg/ml for F, L, and men, respectively). The plasma osmolality threshold for AVP release was lowest in L (x-intercept, 263 +/- 3 mosmol/kgH(2)O, P < 0.05) compared with F (273 +/- 2 mosmol/kgH(2)O) and men (270 +/- 4 mosmol/kgH(2)O) during HSI. Men had greater P([AVP])-plasma osmolality slopes (i.e., sensitivity) compared with F and L (slopes = 0.14 +/- 0.04, 0.09 +/- 0.01, and 0.24 +/- 0.07 for F, L, and men, respectively, P < 0.05). Despite similar Na+-regulating hormone responses, men excreted less Na+ during HSI (0.7 +/- 0.1, 0.7 +/- 0.1, and 0.5 +/- 0.1 meq/kg body wt for F, L, and men, respectively, P < 0.05). Furthermore, men had greater systolic blood pressure (119 +/- 5, 119 +/- 5, and 132 +/- 3 mmHg for F, L, and men, respectively, P < 0.05) than F and L. Our data indicate greater sensitivity in P([AVP]) response to changes in plasma osmolality as the primary difference between men and women during HSI. In men, this greater sensitivity was associated with an increase in systolic blood pressure and pulse pressure during HSI, most likely due to a shift in the pressure-natriuresis curve.     

The influence of gestational age and onset of labour on determinants of fetal-maternal fluid and electrolyte balance in sheep.

Our aim was to compare the effects of gestational age and the timing of the onset of labour on factors influencing fetal fluid and electrolyte balance and urine production in fetal sheep. We measured the volume and composition of fetal urine and amniotic and allantoic fluids, as well as fetal and maternal plasma composition and micturition episodes in sheep during late gestation until the onset of labour. We found that daily fetal urine production and urethral urine flow per micturition episode increased significantly in relation to the onset of labour but not to gestational age (P < 0.05). In the 2 days preceding the onset of labour fetal urine and amniotic fluid K+ concentrations and urine osmolality increased significantly and the Na+/K+ ratio in allantoic fluid decreased significantly (P < 0.05). There was also a significant fall in fetal arterial SaO2 (P < 0.05) but no significant changes occurred in fetal plasma electrolyte composition, osmolality or AVP concentrations. Fetal plasma cortisol and prolactin concentrations and amniotic and allantoic fluid prolactin concentrations increased significantly and progressively in association with both advancing gestation and the onset of labour whereas maternal plasma prolactin concentrations increased significantly only in the 2 days before the onset of labour (P < 0.05). We conclude that some developmental aspects of fetal fluid and electrolyte balance, including renal function, are more closely related to the timing of parturition than to gestational age per se.     

Cortisol effect on atrial natriuretic factor response to hypertonic saline in fetal sheep.

Atrial natriuretic factor (ANF) is released following a variety of stimuli including hypertonicity in the fetus. To study the effect that cortisol has on fetal ANF release, seven chronically instrumented fetal sheep at gestational ages ranging from 110-132 days were studied in two experiments. In one experiment (CORTISOL), a continuous cortisol (with EtOH vehicle) infusion was maintained. In the other experiment (CONTROL), the vehicle was infused alone. Ninety minutes from the start of this infusion, a hypertonic saline bolus (12 meg/kg) was given. Osmolality, ANF, cortisol, pH, PO2, PCO2, mean arterial pressure (MAP), heart rate (HR), and hematocrit (HCT) were followed over a 120-min period. Following hypertonic saline, serum osmolality increased from 290.6 +/- 2.3 mOsm/kg to 310.4 +/- 2.5 mOsm/kg (P < 0.01). Baseline values for pH, PO2, and HCT were 7.37 +/- 0.01, 22.5 +/- 1.6 mmHg, and 33.9 +/- 1.2 respectively. Each of these variables fell following hypertonic saline infusion. MAP rose from 40.6 +/- 1.7 mmHg to 47.0 +/- 2.4 mmHg (P < 0.01). However, there were no differences between CONTROL and CORTISOL experiments in any of the above changes. Cortisol levels in the CONTROL group did not change during the course of the experiment, but in the CORTISOL group rose from 8.2 +/- 4.4 ng/ml to 33.0 +/- 9.9 ng/ml (P = 0.02). Plasma ANF levels prior to hypertonic saline were similar (124.8 +/- 17.7 pg/ml and 127.6 +/- 26.1 pg/ml) in the CONTROL and CORTISOL groups respectively and rose following hypertonic saline to a maximum of 155.3 +/- 16.6 pg/ml and 189.2 +/- 42.7 pg/ml (P = 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Vasopressin and nitric oxide synthesis after three days of water or food deprivation

Nitric oxide has been suggested to be involved in the regulation of fluid and nutrient homeostasis. In the present investigation, vasopressin and nitric oxide metabolite (nitrite and nitrate) levels were determined in plasma of male Wistar rats submitted to water or food deprivation for three days. Hematocrit and plasma sodium showed marked increase in dehydrated and starved rats. Potassium levels and plasma volume decreased in both treated groups. Plasma osmolality and vasopressin levels were significantly elevated in water deprived (362.8 +/- 7.1 mOsm/kg H2O, 17.3 +/- 2.7 pg/ml, respectively, p < 0.001) rats, but not in food deprived (339.9 +/- 5.0, 1.34 +/- 0.28) rats, compared to the controls (326.1 +/- 4.1, 1.47 +/- 0.32). The alterations observed in plasma vasopressin levels were related to plasma osmolality rather than plasma volume. Plasma levels of nitrite and nitrate were markedly increased in both water and food deprived rats (respectively, 2.19 +/- 0.29 mg/l and 2.22 +/- 0.17 mg/l versus 1.33 +/- 0.19 mg/l, both p < 0.01). There was a significant negative correlation between plasma nitrite and nitrate concentration and plasma volume. These results suggest that both dehydration and starvation increase plasma nitric oxide, probably by activation of nitric oxide synthases. The release of nitric oxide may participate in the regulation of the alteration in blood flow, fluid and nutrient metabolism caused by water deprivation or starvation.     

Effects of high altitude and water deprivation on arginine vasopressin release in men

High-altitude exposure changes the distribution of body water and electrolytes. Arginine vasopressin (AVP) may influence these alterations. The purpose of this study was to examine the effect of a 24-h water deprivation trial (WDT) on AVP release after differing altitude exposures. Seven healthy males (age 22 +/- 1 yr, height 176 +/- 2 cm, mass 75.3 +/- 1.8 kg) completed three WDTs: at sea level (SL), after acute altitude exposure (2 days) to 4,300 m (AA), and after prolonged altitude exposure (20 days) to 4,300 m (PA). Body mass, standing and supine blood pressures, plasma osmolality (Posm), and plasma AVP (PAVP) were measured at 0, 12, 16, and 24 h of each WDT. Urine volume was measured at each void throughout testing. Baseline Posm increased from SL to altitude (SL 291.7 +/- 0.8 mosmol/kgH2O, AA 299.6 +/- 2.2 mosmol/kgH2O, PA 302.3 +/- 1.5 mosmol/kgH2O, P < 0.05); however, baseline PAVP measurements were similar. Despite similar Posm values, the maximal PAVP response during the WDT (at 16 h) was greater at altitude than at SL (SL 1.7 +/- 0.5 pg/ml, AA 6.4 +/- 0.7 pg/ml, PA 8.7 +/- 0.9 pg/ml, P < 0.05). In conclusion, hypoxia appeared to alter AVP regulation by raising the osmotic threshold and increasing AVP responsiveness above that threshold.     

Effects of dehydration on the vasopressin response to immersion

Nine healthy volunteers underwent three experimental procedures in random order. The protocols were 4 h of thermal dehydration followed by 2 h of head-out water immersion, 4 h of thermal dehydration followed by 2 h of chair rest, and 6 h of rest in the supine position. Four hours of heat exposure (50 degrees C) resulted in a body weight loss of approximately 3.5%. Plasma osmolality rose by approximately 5 mosmol/kg, mean arterial pressure (MAP) decreased from 85 to 78 mmHg, and body temperature increased from 36.8 to 38.6 degrees C. As a consequence of the combined action of hypertonicity, hypovolemia, hypotension, and hyperthermia, plasma arginine vasopressin (AVP) increased from 2.1 to 8.1 pg/ml after 4 h thermal dehydration. Changes in body weight, plasma osmolality, body temperature, and MAP were similar after either a subsequent 2 h of water immersion or 2 h of chair rest. However, during chair rest plasma AVP remained elevated (8.4 pg/ml), whereas during immersion plasma AVP decreased from 8.1 to 4.7 pg/ml. This was probably due to the central hypervolemia induced by immersion. Our results support the hypothesis that central hypervolemia rather than hypotonicity is the primary stimulus for AVP suppression during water immersion in dehydrated subjects. During the early immersion period hypoosmolality might contribute to the AVP suppression.     

Plasma levels of arginine vasotocin,prolactin, aldosterone and corticosterone during prolonged dehydration in the domestic flowl: effect of dietary NaCl

Three groups of White Plymouth Rock laying hens were adapted to three levels of dietary NaCl: low-NaCl food with tap water (LOW), high-NaCl food (1% NaCl w/w added) with tap water (HT), and high-NaCl food with 0.5% NaCl for drinking (HS). The birds were subjected to water deprivation (dehydration) for 18 days. Blood sampling was done at 2-4 day intervals. Plasma concentrations of arginine vasotocin (AVT), prolactin (PRL), aldosterone (ALDO) and corticosterone (CS) were determined by radioimmunoassay. Plasma osmolality, sodium, chloride, and potassium were also determined. In the normally hydrated hens fully adapted to the diets, there was a stepwise increase from LOW to HS in plasma osmolality (305, 315, 332 mOsm, for LOW, HT and HS, respectively), [Na+] (144, 153, 161 mM) and [Cl-] (109, 119, 127 mM) as well as in [AVT] (6, 14, 18 pg/ml) and [PRL] (16, 24, 34 ng/ml). Regressing [AVT] on osmolality gave a slope of 0.30 pg . ml-1/mOsm and a threshold of 273 mOsm. The slope of [PRL] on osmolality was 0.73 ng . ml-1/mOsm. The correlation coefficient of [AVT] and [PRL] was 0.67. LOW had high [ALDO] (165 pg/ml) which was suppressed to low levels in HT and HS (5-8 pg/ml), while [CS] was the same in all groups (0.9-1.1 ng/ml). Plasma [K+] was decreased in the high-NaCl groups (5.8 mM in LOW, 4.4 and 4.7 mM in HT and HS). Dehydration resulted within 2 days generally in a sharp (5-15%) increase in osmolality, [Na+] and [Cl-], which thereafter increased more slowly during the remaining 16 days in all groups, with the slowest increase in LOW. The levels of osmolality [Na+] and [Cl-] were 5% lower in LOW than in HT and HS, which showed the same levels during the dehydration period. Plasma [AVT] and [PRL] increased 2-4 fold within 2 days of dehydration; [AVT] reached a plateau at 29 pg/ml in all groups, but [PRL] continued to rise in all groups, fastest in LOW, reaching similar levels in all groups after 14-18 days of dehydration, about 85 ng/ml. The correlation coefficient of [AVT] and [PRL] was decreased by half (to 0.32) during dehydration. Plasma [ALDO] increased in all groups with dehydration, 1.7 fold in LOW and 3-6 fold in HT and HS, but the levels reached in HT and HS were only 15-30% of that seen in LOW.(ABSTRACT TRUNCATED AT 400 WORDS)     

Vasopressin and A1 noradrenaline turnover during food or water deprivation in the rat

In the present study, we have examined in Wistar rats the effects of food or water deprivation of 3 days on the hypophyso-adrenal axis, vasopressinergic system and activity of A1 noradrenergic brain stem cell group, which is involved in the control of the hypothalamic neuro-endocrine activity. Levels of adrenocorticotropic hormone (ACTH) and vasopressin (AVP) were determined by radio-immunoassay, and corticosterone level was determined by fluorimetric method. Plasma levels of ACTH and corticosterone were greatly increased in both groups of rats. In water-deprived rats, plasma AVP (13.83 +/- 1.63 vs. 3.03 +/- 0.23 pg/ml) and osmolality levels were significantly elevated with a marked decrease of AVP hypophysis content (272 +/- 65 vs. 1098 +/- 75 ng/mg protein), but not in food-deprived rats in which osmolality did not change and AVP remained stocked (2082 +/- 216 ng/mg protein) in the hypophysis without release in the plasma (1.11 +/- 0.23 pg/ml). These observations indicated that both food-deprivation and water-deprivation stimulated the pituitary adrenal axis thereby suggesting a stress state. AVP production is stimulated both by fluid and food restriction but is secreted with differential effects: during food restriction AVP secretion is limited to supporting the hypothalamic pituitary-adrenal system.     

Plasma vasopressin and aldosterone responses to oral and intravenous saline rehydration.

This investigation examined plasma arginine vasopressin (AVP) and aldosterone (Ald) responses to 1) oral and intravenous (IV) methods of rehydration (Rh) and 2) different IV Rh osmotic loads. We hypothesized that AVP and Ald responses would be similar between IV and oral Rh and that the greater osmolality and sodium concentration of a 0.9% IV saline treatment would stimulate a greater AVP response compared with a 0.45% IV saline treatment. On four occasions, eight men (age: 22.1 +/- 0.8 yr; height: 179.6 +/- 1.5 cm; weight: 73.6 +/- 2.5 kg; maximum O(2) consumption: 57.9 +/- 1.6 ml. kg(-1). min(-1), body fat: 7.7 +/- 0.9%) performed a dehydration (Dh) protocol (33 degrees C) to establish a 4-5% reduction in body weight. After Dh, subjects underwent each of three randomly assigned Rh (back to -2% body wt) treatments (0.9 and 0.45% IV saline, 0.45% oral saline) and a no Rh treatment during the first 45 min of a 100-min rest period. Blood samples were obtained pre-Dh, immediately post-Dh, and at 15, 35, and 55 min post-Rh. Before Dh, plasma AVP and Ald were not different among treatments but were significantly elevated post-Dh. In general, at 15, 35, and 55 min post-Rh, AVP, Ald, osmolality, and plasma volume shifts did not differ between IV and oral fluid replacement. These results demonstrated that the manner in which plasma AVP and Ald responded to oral and IV Rh or to different sodium concentrations (0.9 vs. 0.45%) was not different given the degree of Dh (-4.5% body wt) and Rh and amount of time after Rh (55 min).     

Effect of rehydration on atrial natriuretic peptide release during exercise in the heat

In an attempt to investigate their relationships with plasma volume (PV), heart rate (HR), and other hormonal systems, plasma atrial natriuretic peptide (ANP) levels were determined in response to exercise in the heat, associated with dehydration and rehydration with various fluids. Five normal subjects underwent four 3-h experiments, in a 36 degree C environment, in which 25-min exercise periods on a cycle ergometer at 90 W alternate with 5-min rest periods. Blood samples were collected hourly and ANP, arginine vasopressin (AVP), adrenocorticotropin (ACTH), and cortisol were analyzed in four experimental sessions: without fluid supplement (DH) and with progressive rehydration either with water (W), acid isotonic solution (AISO), or neutral isotonic solution (NISO). Exercise in the heat, accompanied by a decrease in PV and an increase in osmolality, elicited an increase of 28 +/- 1.6 pg/ml in plasma ANP, with concomitant increases in AVP (5.1 +/- 1.4 pg/ml), ACTH (49.6 +/- 12.3 pg/ml), and cortisol (8.4 +/- 2.0 micrograms/100 ml). Progressive rehydration maintained PV and blunted ANP, AVP, ACTH, and cortisol responses. These results demonstrate the importance of rehydration, during exercise in a warm environment, in preventing hormonal increases. They suggest that under our conditions, the PV changes and the inferred atrial pressure changes may not be the primary factors controlling ANP release, as under other physiological conditions. The exercise-related activation of pituitary and adrenals and the stimulation of HR counteract the influence of PV changes due to vascular fluid shifts.     

Fetomaternal adrenomedullin levels in diabetic pregnancy.

We investigated whether maternal and fetoplacental adrenomedullin, a newly discovered hypotensive peptide involved in the insulin regulatory system, is modified in diabetic pregnancy. We studied its correlation with pregnancy complications associated with this disease. Thirty-six pregnant women with diabetes (13 with type I and 23 with gestational diabetes mellitus) and in 40 uncomplicated pregnancies were included. 10 out of 36 diabetic pregnancies were complicated by gestational hypertension. In each woman, adrenomedullin concentration in maternal and fetal plasma and in amniotic fluid was assessed by specific radioimmunoassay. We found that overall mean amniotic fluid adrenomedullin concentration was higher (p < 0.05) in diabetic (14.7 +/- 1.6 fmol/ml) than in uncomplicated pregnancies (10.8 +/- 0.9 fmol/ml), whereas no differences were present in maternal and fetal plasma adrenomedullin levels between diabetic and uncomplicated pregnant women. High levels of amniotic fluid adrenomedullin were found in both type I and gestational diabetes mellitus pregnancies (13.7 +/- 1.4 and 15.6 +/- 2.2 fmol/ml, respectively). Diabetic pregnancies complicated by gestational hypertension showed lower (p < 0.05) amniotic fluid adrenomedullin concentrations than normotensive diabetic patients. These findings suggest that placental adrenomedullin production is upregulated in diabetic pregnancy, and it may be important to prevent excessive vasoconstriction of placental vessels.     

Plasma arginine vasotocin and angiotensin II in the water deprived Kelp gull (Larus dominicanus), Cape gannet (Sula capensis) and Jackass penguin (Spheniscus demersus)

1. The basal levels of the osmoregulatory hormones, arginine vasotocin (AVT) and angiotensin II (AII) were measured (by radioimmunoassay) in the plasma of conscious Kelp gulls, Cape gannets and Jackass penguins. 2. The responses of the hormones to similar degrees of hypertonicity and hypovolemia caused by water deprivation have also been determined. 3. Dehydration elevated plasma AVT and plasma AII in all three species. 4. The AVT concentration was increased by 2-4 fold and although in each case the correlation between plasma osmolality and plasma AVT was highly significant (2P less than 0.01), the sensitivity of release was greater in the gull (1.13 pg/ml per mOsm/kg) than in the gannet (0.36 pg/ml per mOsm/kg) or penguin (0.44 pg/ml per mOsm/kg). 5. Dehydration increased plasma AII 3-fold in the three bird types.     

Absorption of amniotic fluid by amniochorion in sheep

Swallowing of amniotic fluid and lung fluid inflow were eliminated in 10 chronically instrumented fetuses. The urachus was ligated, and fetal was urine drained to the outside. At the beginning and the end of 21 experiments of 66 +/- 5 (SE) h duration, all amniotic fluid was temporarily drained to the outside for volume measurement and sampling. Amniotic fluid osmolalities and oncotic pressures were experimentally controlled. Amniochorionic absorption of amniotic fluid depended strongly on the osmolality difference between amniotic fluid and fetal plasma (P < 0.001), but at zero osmolality difference there still was a mean absorption rate of 23.8 +/- 4.7 (SE) ml/h (P < 0.001). Absorption was unaffected by the protein concentration difference between amniotic fluid and fetal plasma, but infused bovine albumin in the amniotic fluid was absorbed at a rate of 1.8 8 +/- 0.4 g/h (P < 0.001), corresponding to a volume flow of fluid of 33.8 8 +/- 6.1 ml/h (P < 0.001). Fluid absorption in the amniochorion is driven in part by crystalloid osmotic pressure, but about 25 ml/h is absorbed by a path that is permeable to protein. That path has the physiological characteristics of lymphatic drainage, although no anatomic basis is known to exist for a lymphatic system in the amniochorion.