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Physiological elevation of plasma vasopressin in man results in a small reduction in skeletal muscle blood flow but the action on skin blood flow has not been reported. We have studied eight male subjects during infusion of arginine vasopressin (AVP) at 2 units/h for 90 min. Plasma levels of AVP, measured by radioimmunoassay, rose to 68.5 (7.0) pg/ml, mean (SEM). Forearm and finger blood flow was measured with an electronic plethysmograph, hand interdigital skin-fold blood flow with a laser-Doppler blood flow meter and facial temperature with a thermocouple. All subjects developed marked facial pallor during infusion of AVP, facial temperature falling from 34.2 (0.2) to 32.7 (0.1) degrees C (P less than 0.001) then rising to 33.7 (0.1) degrees C (P less than 0.01) after AVP was stopped. Hand interdigital skin-fold blood flow also fell from 2.6 (0.02) to 2.3 (0.02) V (P less than 0.001) and rose sharply to 3.6 (0.2) V (P less than 0.001) on stopping the infusion. There were small changes in forearm and finger blood flow: both rose, from 6.3 (0.1) to 6.9 (0.1) (P less than 0.001) and 46.1 (1.0) to 54.3 (0.7) ml min-1 100 ml-1 (P less than 0.001) respectively. Neither fell when AVP was stopped. Heart rate remained unchanged throughout. These results indicate that high physiological levels of AVP, comparable with those attained during physical stress, produced a fall in blood flow in the face and interdigital skin-fold of the hand consistent with a fall in nutritional blood flow to skin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The differential effect of arginine vasopressin on skin blood flow in man. 379 64

We studied prospectively eight healthy postpartum breast-feeding women for 6 months during early, middle, and late lactation. Blood for measurement of oxytocin (OT), PRL, and arginine vasopressin was drawn before and every 3 min from each women during 15 min of infant suckling for two consecutive feedings during each stage of lactation. Basal plasma OT was not different in breast-feeding [0.7 +/- 0.1 (+/- SEM) microU/ml] and nonbreast-feeding women (0.8 +/- 0.2 microU/ml). OT increased significantly in response to infant suckling (P less than 0.00001) to 5.9 +/- 0.5 microU/ml and remained elevated throughout a feeding. OT was released during infant suckling in an episodic pattern in some, but not all, women; peak OT varied among women (5.0-23.3 microU/ml). There was no significant difference in the mean stimulated OT or the pattern of release comparing the first and second feedings of the same day. The mean OT (n = 8) released during 15 min of infant suckling was not significantly different in early (3.9 +/- 0.3 microU/ml), middle (4.5 +/- 0.3 microU/ml), and late (5.8 +/- 0.4 microU/ml) lactation. In the four women who breast fed exclusively, the mean stimulated OT was significantly higher (P less than 0.01) during late lactation (8.6 +/- 0.4 microU/ml) vs. early (4.6 +/- 0.4 microU/ml) or middle (6.1 +/- 0.4 microU/ml) lactation. In the other four women who provided formula supplements, OT did not change. Plasma arginine vasopressin did not increase in response to infant suckling. Plasma PRL increased in response to infant suckling, reaching a peak at 15 min. Mean basal PRL decreased progressively from weeks 1-24 postpartum. Mean peak PRL decreased significantly from early (162 +/- 29) to middle (130 +/- 15) to late (77 +/- 10) ng/ml lactation (P less than 0.05). OT release in response to infant suckling continues throughout the first 6 months postpartum in breast-feeding women, and the pattern is reproducible. The maximum release of OT is dependent upon continuous regular nipple stimulation. In contrast to basal and suckling-induced levels of PRL, which decreased with time postpartum, basal and suckling-induced OT release did not decrease from early to late lactation.
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PMID:A prospective longitudinal study of the release of oxytocin and prolactin in response to infant suckling in long term lactation. 394 49

The posterior pituitary response to immobilization was studied in male and female rats. Plasma levels of arginine vasopressin (AVP) and oxytocin (OT) were measured both in control rats and in rats immobilized in an acrylic restrainer for 1 min. In male rats immobilization did not result in any change in AVP (control: 1.3 +/- 0.2 pmol/liter, mean +/- SEM; immobilized: 2.3 +/- 0.6 pmol/liter), although there was a small but significant increase in OT (control; 4.1 +/- 0.5 pmol/liter; immobilized: 10.2 +/- 2.2 pmol/liter; P less than 0.005). In female rats a marked rise was observed in AVP (control: 1.4 +/- 0.3 pmol/liter; immobilized: 5.5 +/- 1.3 pmol/liter; P less than 0.005), and the rise in OT was considerably greater (P less than 0.01) than that found in males (control: 4.7 +/- 0.8 pmol/liter; immobilized: 26.0 +/- 5.6 pmol/liter; P less than 0.001). Further groups of male and female rats were gonadectomized 2 weeks before immobilization. Basal levels of AVP and OT were unchanged. Orchidectomized males had an increased OT response to immobilization compared with sham-operated males (P less than 0.05) whereas the AVP response was not significantly changed. Ovariectomy did not significantly affect either the AVP or OT responses. Although the neural pathways responsible for the neurohypophyseal response to immobilization are not known, this data demonstrate that the response is dependent on the sex of the rat.
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PMID:Sexual dimorphism in the posterior pituitary response to stress in the rat. 396 25

We previously reported a prominent diurnal rhythm of oxytocin (OT) in human cerebrospinal fluid (CSF) similar to the brisk CSF OT rhythm in monkeys. An OT CSF rhythm has not been found in lower species. In contrast, a pronounced arginine vasopressin (AVP) rhythm has been found in lower species, but the AVP CSF rhythm is less marked in subhuman primates. In patients (n = 7) in whom lumbar drains had been temporarily placed for treatment of CSF rhinorrhea, we obtained CSF samples every 6 h. In 6 of these 7 patients, we previously reported (1) finding a prominent CSF OT rhythm, with a peak at 1200 h, by analysis of variance of repeated measures. When the samples of CSF of these same 6 patients (plus 1 additional patient) were assayed for AVP, no AVP rhythm was found. We also measured AVP, OT, and arginine vasotocin (AVT) by RIA in single samples of CSF obtained from 23 other patients. In these single samples of CSF, mean AVP was 0.9 +/- 0.11 (+/- SEM) pg/ml, and OT was 3.7 +/- 0.5 microU/ml. CSF AVT immunoreactivity was 0.6 pg/ml or less in the 23 patients. Two pools of CSF were separated by reverse phase high pressure liquid chromatography. The peak OT and AVP, as determined by RIA, coeluted exactly with synthetic and human posterior pituitary OT and AVP, respectively. No immunoreactive AVT was found in the position of synthetic AVT in the eluates. Thus, OT and AVP are present in human adult CSF, but AVT is not. The lack of a prominent rhythm of AVP in human CSF is in marked contrast to the brisk OT rhythm. The rhythm of neurohypophysial peptides in human and subhuman primates is different from the rhythm in lower species, suggesting different functions for OT and AVP in the central nervous system of various species.
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PMID:Neurohypophysial hormones in cerebrospinal fluid of adults: absence of arginine vasotocin and of a diurnal rhythm of arginine vasopressin. 404 Sep 25

The effect of arginine vasopressin (ADH) on water permeability and transepithelial voltage was examined in cortical collecting tubules from a specific pathogen-free line of male Sprague-Dawley rats (75-125 g body weight). Tubules were bathed in a medium resembling serum ultrafiltrate (310 mOsm/kg H2O) at 38 degrees C. Osmotic water permeability (Pf, micron/sec) was determined by the volume flow occurring with a hypo-osmotic perfusate (210-220 mOsm/kg H2O) and diffusional water permeability (Pd, micron/sec) was calculated from the lumen-to-bath flux of tritiated water using an isosmotic perfusate. In the absence of ADH, both Pf and Pd were low, 17 +/- 6 and 9.0 +/- 0.6 (SEM), respectively. ADH added to the bath at concentrations above 0.5 microunits/ml increased Pf, with a maximal response at 40 microunits/ml or greater. With 100 microunits/ml ADH, Pf and Pd were, respectively, 994 +/- 117 and 37.0 +/- 2.4. Without ADH, the transepithelial voltage was variable (range, -5.4 to +2.5 mV; mean, -1.9 +/- 0.4); however, with 100 microU/ml ADH, it hyperpolarized (lumen-negative) by 4.2 +/- 0.8 mV. In contrast to findings in the rabbit, both the hyperpolarization and the increased water permeability persisted for at least 3 hr. The higher water permeabilities are consistent with the shorter length of the cortical collecting tubule in the rat, and may reflect the importance of attaining osmotic equilibration within the cortex during maximal antidiuresis.
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PMID:Sustained response to vasopressin in isolated rat cortical collecting tubule. 609 38

1. In six healthy volunteer subjects polydipsic water loading significantly increased urine volume from 1203 +/- 242 (SEM) to 5072 +/- 320 ml/24 h (P less than 0.001) with a significant decrease in urinary osmolality. This increase in urine volume by more than fourfold was associated with a slight increase in urinary excretion of prostaglandin E2 from 466 +/- 66 to 1017 +/- 174 pmol/24 h (P = 0.05). 2. In five patients with central diabetes insipidus mean urine volume of 10 838 +/- 107 ml/24 h was reduced to 1205 +/- 204 ml/24 h (P less than 0.001) by treatment with 1-desamino-8-arginine vasopressin (desamino-[Arg8]vasopressin; 15 microgram/day) with a significant rise in urinary osmolality. Desamino-[Arg8]vasopressin treatment was associated with a significant increase of suppressed urinary excretion of prostaglandin E2 (PGE2) in four of these patients from 246 +/- 66 to 2643 +/- 677 pmol/24 h (P less than 0.01). 3. Concomitant treatment with indomethacin in addition to desamino-[Arg8]vasopressin significantly suppressed urinary excretion of PGE2 and significantly increased urinary osmolality as compared with treatment with desamino-[Arg8]vasopressin alone. 4. Desamino-[Arg8]vasopressin significantly increased urinary excretion of adenosine 3':5'-cyclic monophosphate (cyclic AMP). However, there was no further change in urinary excretion of cyclic AMP during concomitant indomethacin treatment. 5. The results suggest that urine flow itself is not an important determinant of urinary PGE2 excretion. In patients with central diabetes insipidus the urinary concentrating response to desamino-[Arg8]vasopressin is enhanced during inhibition of prostaglandin synthesis without changes in urinary excretion of cyclic AMP.
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PMID:Renal prostaglandins and water balance: studies in normal volunteer subjects and in patients with central diabetes insipidus. 626 42

Activation of the sympathetic nervous system, manifested by an increase in heart rate and circulating plasma norepinephrine, can occur in normal subjects when they are given vasodilators. The extent to which this activation occurs in patients with congestive heart failure (CHF) and whether this activation could account for the hemodynamic rebound sometimes observed following abrupt withdrawal of nitroprusside in such patients are unclear. We prospectively and retrospectively studied the effects of nitroprusside on plasma norepinephrine in 38 patients with CHF to determine if acute vasodilator therapy activates this vasoconstrictor system during or following such treatment. Thirty-six of these patients also had plasma renin activity (PRA) measured and plasma arginine vasopressin was measured in 12 patients. Baseline supine plasma norepinephrine (714 +/- 72 pg/ml, +/- SEM), PRA (15 +/- 2 ng/ml/hr), and arginine vasopressin (10 +/- 1 pg/ml) were increased at least twofold in the CHF patients. Nitroprusside (96 +/- 11 micrograms/min) was infused for 63 +/- 5 minutes after achieving an optimal hemodynamic response: cardiac index increased (2.01 +/- 0.08 to 2.67 +/- 0.1 L/min/m2, p less than 0.001), pulmonary artery wedge pressure decreased (25 +/- 1 to 16 +/- 1 mm Hg, p less than 0.001), mean arterial pressure decreased (83 +/- 1 to 72 +/- 1 mm Hg, p less than 0.001), and heart rate was unchanged. Plasma norepinephrine (632 +/- 43 pg/ml), PRA (18 +/- 3 ng/ml/hr), and arginine vasopressin (11 +/- 1 pg/ml) did not change significantly for the group during peak effect of the vasodilator.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The acute response of plasma norepinephrine, renin activity, and arginine vasopressin to short-term nitroprusside and nitroprusside withdrawal in patients with congestive heart failure. 635 44

The effect of hypoxemia on arginine vasopressin (AVP) and oxytocin (OT) release was investigated in the chronically catheterized fetus and ewe. During 30 min of 10% maternal oxygen delivery, mean (+/- SEM) arterial PO2 decreased from 105 +/- 10.6 to 48 +/- 3.5 mm Hg in the ewe and from 21 +/- 1.3 to 12 +/- 0.8 mm Hg in the fetus (each P less than 0.001). Arterial PCO2 decreased from 35 +/- 4.4 to 29 +/- 1.0 mm Hg in the ewe, whereas fetal PCO2 decreased from 43 +/- 2.3 to 35 +/- 3.5 mm Hg (P less than 0.05). Blood pH increased from 7.44 +/- 0.03 to 7.56 +/- 0.04 in the ewe (P less than 0.01) and from 7.36 +/- 0.004 to 7.40 +/- 0.006 in the fetuses (P less than 0.01). Baseline mean AVP levels were identical in ewes and fetuses (0.7 +/- 0.1 microU/ml). After 30 min of hypoxia, plasma AVP levels remained unchanged in the ewes (0.9 +/- 0.1), but increased dramatically in the fetuses (47 +/- 21 microU/ml) (P less than 0.001). There was a highly significant correlation between the duration of hypoxia and log fetal AVP concentrations (r = 0.85). The log fetal plasma AVP also was inversely correlated to the log fetal PO2 values (r = 0.83). Mean baseline fetal and maternal plasma OT levels were 2.6 +/- 0.5 microU/ml and 2.2 +/- 0.5 microU/ml, respectively. After 30 min of hypoxia fetal and maternal OT values were 2.9 +/- 0.8 microU/ml (not significant).
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PMID:The effect of hypoxia on neurohypophyseal hormone release in fetal and maternal sheep. 642 35

A new method of measuring vasopressin activity is described. It depends on the finding that the Na+-K+-ATPase activity, measured cytochemically, in the thick ascending limb of the loop of Henle in rat renal tissue maintained in vitro, responded to increasing concentrations of synthetic arginine vasopressin in a log-dose related fashion. The limit of sensitivity was 0.002 pg/ml (2 x 10(-15) mol/l). The dose-responses were reproducible; the inter-assay coefficient of variation was 6.4% at a vasopressin concentration of 0.02 pg/ml. Normal plasma stimulated this Na+-K+-ATPase activity, the stimulation being reduced by 98% when the plasma had been treated with an antiserum specific for vasopressin. Measured in this system, the circulating levels of plasma vasopressin, in healthy adults after 18h dehydration, was 4.0 +/- 0.3 pg/ml (mean +/- SEM; n = 4) and fell to 0.6 +/- 0.1 pg/ml following a water load. Absolute plasma vasopressin values obtained by the cytochemical bioassay were comparable to those measured by radioimmunoassay (r = +0.97, p less than 0.001).
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PMID:A cytochemical bioassay for arginine vasopressin: preliminary studies. 645 47

Urinary clearance of antidiuretic hormone (ADH) has been measured under basal conditions and during intravenous administration of arginine vasopressin in ten healthy subjects, and only under basal conditions in 18 patients with chronic renal failure and seven patients with acute renal failure at the polyuric phase of the disease. In healthy subjects studied under conditions of mild water diuresis plasma concentration, urinary excretion rate, urinary clearance and fractional clearance of ADH were 3.3 +/- 0.36 pg/ml, 25.2 +/- 5.5 pg/min, 7.5 +/- 1.2 ml/min and 6.4 +/- 1.0% (means +/- SEM) respectively. When plasma ADH was raised to levels between 7 and 26 pg/ml during intravenous administration of the hormone, urinary excretion rate and urinary clearance of ADH increased. Tubular reabsorption of ADH did not reach a plateau but progressively increased in the range of plasma ADH studied. In patients with chronic renal failure, plasma concentration, urinary excretion rate, urinary clearance and fractional clearance of ADH were 2.8 +/- 0.19 pg/ml, 9.4 +/- 2.0 pg/min, 3.4 +/- 0.6 ml/min and 10.0 +/- 2.9% (means +/- SEM) respectively. Urinary excretion rate and urinary clearance were significantly lower than in healthy subjects. In patients with acute renal failure, plasma concentration, urinary excretion rate, urinary clearance and fractional clearance of ADH were 4.6 +/- 0.47 pg/ml, 52.8 +/- 15.8 pg/min, 9.5 +/- 2.7 ml/min and 24.9 +/- 4.4% (means +/- SEM) respectively. Urinary excretion rate and fractional clearance were higher than in healthy subjects and patients with chronic renal failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal excretion of antidiuretic hormone in healthy subjects and patients with renal failure. 646 34

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