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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Nineteen patients with a spectrum of immunologically related disorders were studied before and immediately after plasmapheresis for changes in plasma aldosterone, insulin and arginine vasopressin (AVP). Renin was also measured in 11 of these patients by direct radioimmunoassay. 125% of the initial plasma volume was replaced, which corresponded to a predicted removal of 72% for any plasma constituent. 2. The initial, final (experimental) and final (predicted) concentrations (means +/- SEM) were 337 +/- 50, 185 +/- 23 and 100 +/- 16 pg/ml respectively for renin, 465 +/- 86, 146 +/- 38 and 124 +/- 22 pmol/l respectively for aldosterone, 218 +/- 35, 69 +/- 11 and 63 +/- 11 pmol/l respectively for insulin, 7.2 +/- 1.9, 6.1 +/- 0.5 and 1.8 +/- 0.2 pmol/l respectively for AVP. The predicted final concentration was calculated from the initial concentration and the fraction of plasma volume exchanged. The experimental final concentration was lower than the initial concentration for renin, aldosterone and insulin (P less than 0.001) but not for AVP. The predicted final concentration was lower than the experimental final concentration for AVP and renin (P less than 0.001) but not for aldosterone and insulin. Plasma volume, osmolality, glucose, sodium and potassium concentrations did not change significantly. 3. The concentrations of renin, aldosterone, insulin and AVP in the removed plasma were 84 +/- 17 pg/ml, 179 +/- 36, 98 +/- 15 and 4.8 +/- 0.7 pmol/l respectively. The amount subtracted expressed as percentage of the total amount present in plasma was markedly greater for AVP than for the three other plasma constituents.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Changes in plasma renin, insulin, aldosterone and arginine vasopressin during plasmapheresis. 331 69

We have recently shown that hydrolysis of labeled angiotensin I in canine brainstem homogenate causes a rapid accumulation of the heptapeptide angiotensin-(1-7) [Ang-(1-7)]. Although this angiotensin fragment has no vasopressor activity, its consistent generation in brain homogenate led us to study its potential neurosecretory effects in the rat hypothalamo-neurohypophysial system (HNS) in vitro. Ang-(1-7) or angiotensin II (Ang II) was added to HNS perifusate in concentrations of 0.04, 0.4, and 4 microM, and release of arginine vasopressin (AVP) during each treatment was quantified as a percentage of the AVP release detected in the preceding collection period. Base-line release of AVP averaged 281 +/- 47 pg per 15 min (mean +/- SEM) in HNS explants (five experiments, five explants per chamber) perifused in Krebs solution at 37 degrees C, after a 1-hr equilibration period. At 0.04 microM, Ang II or Ang-(1-7) did not stimulate AVP release. Ang II increased AVP release over the control value by 172% +/- 44% and 268% +/- 66% at 0.4 and 4 microM, respectively; the same concentrations of Ang-(1-7) increased AVP release by 134% +/- 12% and 216% +/- 45%. The responses to Ang II and Ang-(1-7) at the highest concentration were both significant (P less than 0.05), and comparison by two-way analysis of variance indicated that Ang II and Ang-(1-7) were equipotent in stimulating AVP release over the range of concentrations studied. In the presence of the competitive Ang II antagonist [Sar1,Thr8]Ang II (20 microM), the release of AVP increased approximately equal to 2-fold. Neither Ang II nor Ang-(1-7) (4 microM) caused a further enhancement of AVP release in the presence of [Sar1,Thr8]Ang II. These data suggest that a hydrophobic residue in position 8 of the angiotensin peptide is not essential for activation of angiotensin receptors in the rat HNS. Moreover, the equipotence of Ang II and Ang-(1-7) indicates that Ang-(1-7) may participate in the control of AVP release.
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PMID:Release of vasopressin from the rat hypothalamo-neurohypophysial system by angiotensin-(1-7) heptapeptide. 337 55

The goal of this study was to examine humoral mechanisms that regulate blood flow to the choroid plexus. We determined the effects of arginine vasopressin on blood flow (microspheres) to the choroid plexus in anesthetized and awake rabbits. In anesthetized rabbits, blood flow to the choroid plexus was 342 +/- 31 (mean +/- SEM) ml/min/100 g under control conditions. Intravenous infusion of vasopressin at 4 and 40 mU/kg increased plasma vasopressin levels from 11 +/- 1 to 55 +/- 15 and 441 +/- 120 pg/ml, respectively, and blood flow to the choroid plexus decreased by 48 +/- 6% and 70 +/- 4%. Cerebral blood flow was not affected by infusion of vasopressin. Similar responses to infusion of vasopressin were observed in awake rabbits. The V1 antagonist [d(CH2)5Tyr(Me)AVP] (10 micrograms/kg i.v.) had no effect on resting blood flow, but abolished the effect of vasopressin on blood flow to the choroid plexus. Vasoconstrictor responses of the choroid plexus to intravenous infusion of phenylephrine were not attenuated by the V1 antagonist. Thus, circulating vasopressin, at plasma levels that are observed under physiological and pathophysiological conditions, has marked effects on blood flow to the choroid plexus. These effects appear to be mediated through a V1 receptor. We speculate that vasopressin may play an important role in regulation of blood flow to the choroid plexus and perhaps in the regulation of cerebrospinal fluid production.
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PMID:Humoral regulation of blood flow to choroid plexus: role of arginine vasopressin. 339 58

The effects of rat CRF, arginine vasopressin (VP), oxytocin (OXY), and isoproterenol (ISO) on the biosynthesis and release of pro-ACTH/endorphin-derived peptides by monolayer cultures of rat anterior pituitary cells in complete serum-free medium (CSFM) were studied. When cells were exposed to hormone for 3 h, CRF, VP, OXY, and ISO were each able to stimulate secretion of immunoactive hormone into culture medium. To determine the effects of chronic secretagogue exposure on corticotrope function, cultures were exposed to hormone for 14 days, and total hormone production was measured by immunoassay (cumulative hormone secreted plus cell hormone content). In the absence of CRF, total hormone production increased 3.6 +/- 0.2-fold (mean +/- SEM) over the period from 2-14 days; chronic CRF treatment brought about a 7.9 +/- 0.7-fold increase in total hormone production over the same period (P less than 0.0025) or a 2.2-fold increase over control cells. Total hormone production was not affected by chronic treatment with VP (100 nM), OXY (100 nM), or ISO (100 nM); the response of the cells to chronic CRF treatment was unaltered by chronic inclusion of VP, OXY, or ISO. To examine the chronic effects of secretagogues more directly, anterior pituitary cells were grown in control CSFM or in CSFM containing CRF or VP for 7 days and then incubated in medium containing radiolabeled amino acid for 15 min. The newly synthesized pro-ACTH/endorphin was quantified by immunoprecipitation and sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). Cells grown in CSFM containing CRF synthesized 1.9 times more labeled pro-ACTH/endorphin that cells grown in control CSFM or in CSFM containing VP. Chronic exposure of anterior pituitary cultures to 8-bromo-cAMP stimulated both synthesis and release of pro-ACTH/endorphin-derived peptides, suggesting that a secretagogue capable of producing a sustained elevation in intracellular cAMP levels will stimulate prohormone synthesis.
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PMID:Effect of chronic secretagogue exposure on pro-adrenocorticotropin/endorphin production and secretion in primary cultures of rat anterior pituitary. 349 70

Blood samples (4 ml) for plasma arginine vasopressin (AVP) measurements were obtained at 3- to 4-hour intervals under basal conditions for 1-2 days from 5 date-bred ewes with chronic maternal and fetal vascular catheters. In addition, 6 chronically catheterized ewes were infused with 2 liters of 0.45% NaCl over 30 min. Fetal and maternal blood samples were obtained before and after the infusion period for measurement of plasma osmolality and AVP concentrations. In the first study, maternal and fetal plasma AVP levels correlated significantly (p less than 0.01, by linear regression analysis) under basal conditions. In the second study, baseline mean (+/- SEM) plasma osmolality was similar for pregnant ewes and fetuses (303 +/- 3.1 and 302 +/- 2.4 mosm/kg, respectively). There was a significant (each, p less than 0.01 by paired t test) decrease from baseline in maternal and fetal osmolality during the 30 min after completion of the hypotonic saline (to 292 +/- 4.7 and 296 +/- 2.4 mosm/kg, respectively). Fetal plasma AVP levels decreased 17 +/- 6% by 30 min following the completion of water loading (1.7 +/- 0.07 to 1.4 +/- 0.16 microU/ml; p less than 0.05). Maternal plasma AVP levels decreased 16 +/- 4% by 30 min after completion of infusion (1.6 +/- 0.14 to 1.38 +/- 0.6 microU/ml; p less than 0.05). These results indicate that maternal and fetal plasma AVP levels correlate under basal conditions and that maternal water loading, which significantly decreases fetal plasma osmolality, significantly suppresses fetal plasma AVP concentrations.
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PMID:Fetal arginine vasopressin under basal and hypoosmolal conditions. 358 Apr 25

The blood pressure (BP) and heart rate (HR) responses to 5 min incremental intravenous infusions of noradrenaline (NA) and arginine vasopressin (AVP) were investigated both in patients with progressive autonomic failure (PAF) and in normal volunteers. Stepwise infusion of NA at rates of 300-3000 pmol min-1 kg-1 produced a bradycardia and a dose related increase in BP in normal subjects. In subjects with PAF there was no significant HR response but the dose-BP response was shifted to the left with significant pressor responses at infusion rates of 60-300 pmol min-1 kg-1. Stepwise infusion of AVP at 0.2-5.0 pmol min-1 kg-1 caused transient bradycardia but no pressor response in seven normal volunteers. Further increases in AVP infusion in three other subjects achieved plasma AVP levels as high as 3000-4000 pmol/l, and still no significant pressor response was observed. Stepwise infusion of AVP at 0.05-2.0 pmol min-1 kg-1 in the eight subjects with PAF resulted in a pressor response without any change in HR. During this infusion plasma AVP increased from 0.8 +/- 0.2 (mean +/- SEM) to 30 +/- 2 pmol/l. A significant pressor response was already apparent at a plasma AVP level of 5.5 +/- 1.8 pmol/l.
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PMID:Pressor effect of arginine vasopressin in progressive autonomic failure. 372 Jan 94

Estrogen-stimulated neurophysin (ESN) or oxytocin (OT)-neurophysin (Np) was measured in plasma of seven men before and after oral administration of 25 mg diethylstilbestrol (DES). Pre-DES levels of ESN averaged 0.93 +/- 0.3 (+/- SEM) ng/ml and increased to 29.8 +/- 6.5 and 25.4 +/- 5.1 ng/ml 24 and 48 h after DES treatment, respectively. To compare the estrogen-responsive Np in plasma with human OT-Np which is present in the posterior pituitary gland, the Np fraction of post-DES plasma was concentrated by double precipitation with ammonium sulfate and applied to ampholyte displacement and Sephadex G-75 columns. The Np fraction of this plasma extract contained ESN immunoreactivity (IR) but no nicotine-stimulated neurophysin-IR. ESN-IR of plasma and of an extract of human posterior pituitary eluted identically from a Sephadex G-75 column, indicating similar mol wt. The plasma extract containing ESN-IR eluted from the ampholyte displacement column at pH 4.3-4.2. No nicotine-stimulated Np (arginine vasopressin-Np)-IR was found in the plasma samples. ESN-IR in an extract of human posterior pituitary gland eluted from the ampholyte displacement column at the same pH as that of the ESN extracted from plasma. Peak ESN-IR-containing fractions from the ampholyte displacement were pooled, dialyzed, lyophilized, and reconstituted in appropriate carrier buffer for reverse phase high pressure liquid chromatography. The ESN-IR was resolved into two distinct ESN-IR peaks by high pressure liquid chromatography. Plasma and posterior pituitary gave identical pairs of peaks. Thus, the Np that is increased in human plasma in response to estrogen is identical to pituitary OT-Np, providing strong evidence that estrogen stimulates the human neurohypophysis.
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PMID:Ampholyte displacement and high pressure liquid chromatographic separation of the estrogen-responsive neurophysin from human plasma. 374 3

The pharmacokinetics in the human of 1-deamino-2-D-Tyr(OEt)-4-Thr-8-Orn-vasotocin (dE-TVT), was studied after iv and intranasal administration in 11 subjects at 12 experiments each route. The plasma concentration of the analogue was analysed by means of an arginine vasopressin antibody, which cross-reacted with dE-TVT to 4.7%. When given intravenously as bolus injection (10 nmol/kg/body weight), the total body clearance amounted to 0.623 +/- 0.099 (SEM) l/h kg and the half-life to 16.2 +/- 2.4 min. After intranasal administration (100 nmol/kg/body weight), the bioavailability was 10.5 +/- 2.9%. Peak concentrations in plasma appeared 2-8 min after iv and 10-45 min after intranasal administration. At the end of an observation period of 2 h measurable amounts in plasma were still found in one of the iv and seven of the intranasal experiments. It is concluded that the moderately long half-life is suitable for the treatment of hospitalized patients in premature labour where promising results with intravenous infusion (50 micrograms/min) of dE-TVT have been obtained. It is still uncertain whether or not the absorption of dE-TVT is sufficient for intranasal administration to out-patients with uterine hyperactivity in late pregnancy and to patients with primary dysmenorrhoea, where significant relief of symptoms were seen after iv administration (10 micrograms/kg body weight).
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PMID:Pharmacokinetics in the human of a new synthetic vasopressin and oxytocin uterine antagonist. 375 61

The effect of circulating arginine vasopressin (AVP) on blood pressure, heart rate and skin blood flow was investigated in 8 untreated patients with mild essential hypertension using a specific antagonist of the pressor effect of AVP. Skin blood flow was measured with a laser Doppler flowmeter and blood pressure with a Remler M2000 recorder. The study was carried out in double-blind fashion using a cross-over design. Each patient received at a 60 min interval the AVP-antagonist, d(CH2)5Tyr(Me) AVP, 5 micrograms/kg i.v., and its vehicle. The sequence of treatment phases was randomly allocated. Pretreatment plasma AVP levels averaged 1.1 +/- 0.2 pg/ml (mean +/- SEM). Neither the AVP-antagonist nor its vehicle had any effect on blood pressure, heart rate and skin blood flow as well as on plasma renin activity and plasma catecholamines. It is therefore concluded that circulating AVP does not contribute to the maintenance of blood pressure in patients with mild essential hypertension and normal plasma AVP levels.
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PMID:Blockade of the vascular effect of vasopressin in patients with mild essential hypertension. 376 22

To assess the influence of late hyponatraemia on the renal responsiveness to endogenous arginine vasopressin (AVP), urinary excretion and plasma concentration of sodium, plasma and urine osmolality, free water clearance, and urinary AVP concentration and excretion were measured in 11 healthy premature infants with a mean birth weight of 1360 g and mean gestational age of 31 weeks. Studies were performed on days 1, 5, and 19. The development of late hyponatraemia was associated with a pronounced decline in urine osmolality, whereas urine flow rate and free water clearance increased significantly. Mean (SEM) urine AVP concentration and excretion also rose significantly from 2.15 (0.31) pg/ml and 0.36 (0.55) pg/min/m2 on the first day to 6.5 (0.96) pg/ml and 3.85 (0.63) pg/min/m2 on the 19th day, respectively. When renal response to AVP was compared at different ages the highest urine osmolality and steepest response curve was observed on the first day. With development of hyponatraemia the renal response became blunted. It is concluded that the limited tubular sodium transport and hyponatraemia hinders the establishment of intrarenal osmotic gradient, impairs renal response to AVP, and prevents excessive water retention and further fall of plasma sodium.
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PMID:Renal response to arginine vasopressin in premature infants with late hyponatraemia. 377 85


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