Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of vasopressin released during Finnish sauna on blood pressure, heart rate and skin blood flow was investigated in 12 healthy volunteers. Exposure to the hot air decrease body weight by 0.6 to 1.25 kg (mean = 0.8 kg, P less than 0.001). One hour after the end of the sauna sessions, plasma vasopressin was higher (1.7 +/- 0.2 pg/ml, P less than 0.01 mean +/- SEM) than before the sauna (1.0 +/- 0.1 pg/ml). No simultaneous change in plasma osmolality, plasma renin activity, plasma norepinephrine, epinephrine, cortisol, aldosterone, beta-endorphin and metenkephalin levels was observed. Despite the slight sauna-induced elevation in circulating vasopressin, intravenous injection of the specific vascular vasopressin antagonist d(CH2)5Tyr(Me)AVP (5 micrograms/kg) 1 h after the sauna had no effect on blood pressure, heart rate or skin blood flow. These data suggest that vasopressin released into the circulation during a sauna session reaches concentrations which are not high enough to interfere directly with vascular tone.
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PMID:Haemodynamic role of vasopressin released during Finnish sauna. 375 60

Concentrations of vasopressin (VP) precursor and oxytocin (OT) precursor mRNA were measured in magnocellular cell groups of the rat hypothalamus by newly developed solution hybridization assays. The assays employed single-stranded 35S-labeled VP-specific and OT-specific DNA probes that were prepared by primer extension on recombinant M13 DNA templates. Solution hybridization assays were standardized by known amounts of cloned DNA. The detection limit was less than 1 pg DNA equivalent of the respective mRNA. In total RNA preparations of microdissected supraoptic nucleus (SON) mean (+/- SEM) basal levels of 1.37 +/- 0.18 pg VP mRNA and 1.95 +/- 0.14 pg OT mRNA were measured. RNA of the microdissected paraventricular nucleus (PVN) contained 0.35 +/- 0.02 pg VP mRNA and 1.77 +/- 0.15 pg OT mRNA. Elevation of plasma osmolality induced by drinking of 2% saline for 25 days resulted in a 1.85-fold increase in VP mRNA levels of the SON and a 1.6-fold increase in VP mRNA levels of the PVN. The solution hybridization assays are suitable tools to study the regulation of VP and OT mRNAs in magnocellular neurons of the brain.
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PMID:Quantitation of vasopressin mRNA and oxytocin mRNA in hypothalamic nuclei by solution hybridization assays. 377 78

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

alpha MSH is present in high concentrations in the intermediate lobe of the fetal pituitary and has been implicated as a regulator of fetal adrenal steroidogenesis and fetal growth. However, there are few data regarding alpha MSH levels in fetal plasma or the control of fetal alpha MSH secretion. We measured alpha MSH immunoactivity in the plasma of chronically catheterized fetal lambs (gestational age, 116-138 days), newborn lambs, and adult sheep both in the baseline state and after dopamine receptor blockade with metoclopramide. The effect of metoclopramide on the release of another proopiomelanocortin-derived peptide, N-acetyl-beta-endorphin (N-acetyl-beta EP), which is synthesized together with alpha MSH in the intermediate lobe, was also studied. Baseline fetal plasma alpha MSH was significantly greater than maternal alpha MSH [35.6 +/- 2.2 (+/- SEM) vs. 10.0 +/- 1.0 pg/ml]. In eight studies in five fetal lambs, alpha MSH rose to a peak level of 121 +/- 23 pg/ml 15 min after metoclopramide administration to the fetus. Simultaneous maternal alpha MSH levels did not change, suggesting that the alpha MSH in fetal plasma was of fetal pituitary origin. Gel filtration of pooled fetal plasma extracts revealed that the alpha MSH immunoactivity eluted in the same position as the alpha MSH standard. Metoclopramide caused the secretion of nearly equimolar amounts of alpha MSH and N-acetyl-beta EP into fetal plasma. In four fetal lambs, basal N-acetyl-beta EP levels of 156 +/- 34 pg/ml rose to 305 +/- 65 pg/ml 15 min after metoclopramide treatment. Metoclopramide also stimulated plasma alpha MSH in newborn and adult sheep. In six newborn lambs, alpha MSH rose from 45.2 +/- 13 to 211 +/- 38 pg/ml 15 min after metoclopramide treatment, whereas in four adult sheep, a basal alpha MSH level of 11.1 +/- 2.2 pg/ml rose to 20.1 +/- 2.7 pg/ml 15 min after metoclopramide. In addition, metoclopramide stimulated fetal and neonatal PRL secretion, but had no effect on plasma vasopressin concentrations or acid-base and blood gas values. These studies indicate that immunoreactive alpha MSH and N-acetyl-beta EP are secreted into ovine fetal plasma and that the secretion of these peptides in the fetus appears to be under tonic dopamine inhibition, as is the case in the adult sheep and newborn lamb.
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PMID:Dopaminergic regulation of alpha-melanocyte-stimulating hormone and N-acetyl-beta-endorphin secretion in the fetal lamb. 380 22

Since current data on vasopressin (AVP) secretion during the early phase of myocardial infarction is not extensive, plasma AVP was measured in 26 patients with acute myocardial infarction. Twelve had an increased AVP concentration (23.2 +/- 7.0 pg/ml; mean +/- SEM) whereas 14 had an AVP level less than 3 pg/ml (1.96 +/- 0.14 pg/ml). The patients with AVP greater than 3 pg/ml had higher heart rate and plasma osmolality than those with AVP less than 3 pg/ml. Blood pressure values were the same in both groups of patients. There was no difference in peak CPK and iso CPK activities between the two groups. Seven patients with AVP greater than 3 pg/ml died within the next few days, while only 1 patient with AVP less than pg/ml died. It thus appears that increased AVP concentration during acute myocardial infarction is associated with a poor prognosis. Whether it is a cause or a consequence of an unfavourable course of myocardial infarction remains to be determined.
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PMID:[Vasopressin in acute myocardial infarct: clinical implications]. 381 98

Although not demonstrated in patients with cirrhosis, it is generally claimed that administration of vasopressin in the form of triglycyl-lysine-vasopressin (glypressin) may prevent untoward systemic effects of this former hormone. The aim of this study was to assess the effects of intravenous administration of 2 mg of glypressin on splanchnic and systemic hemodynamics in 9 patients with cirrhosis under stable circulatory conditions. One hour after the injection, the following statistically significant changes were observed as compared to the baseline values (m +/- SEM): wedged hepatic venous pressure, -9 +/- 2 p. 100; hepatic venous pressure gradient, -16 +/- 3 p. 100; azygos blood flow, -24 +/- 6 p. 100; heart rate, -16 +/- 3 p. 100; cardiac index, -23 +/- 2 p. 100; systemic vascular resistances, +47 +/- 11 p. 100; wedged pulmonary arterial pressure, +44 +/- 15 p. 100. In conclusion, in patients with cirrhosis in a stable hemodynamic condition, intravenous administration of glypressin decreased portal venous pressure and blood flow into the superior portal systemic collateral circulation but did not prevent the untoward systemic hemodynamic effects of vasopressin.
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PMID:[Effects of glypressin on the splanchnic and systemic circulation in patients with cirrhosis]. 383 Aug 1

To determine the relative importance of central and peripheral osmoreceptors in the osmotically-induced vasopressin secretion, osmosensitive areas of pentobarbital-anaesthetized rats were exposed for 5 sec to an osmotic pulse (130 mumoles NaCl in 200 microliters). The hepatic portal receptors were stimulated by superfusion of the portal vein, and the central receptors by infusion into one common carotid artery. Portal stimulation was 2.14 +/- 0.25 (mean +/- SEM, 4 groups of 5 rats) more effective than central osmotic pulse stimulation in elevating, within 1 minute, the plasma vasopressin level (measured by RIA). The central stimulus was not effective when introduced into the freely perfused vessel, although the hypothalamic extracellular NaCl concentration rose transiently (6 sec) to 2.6 +/- 0.3 w/v% (mean +/- SEM, n = 6 rats). The results show that brief osmotic pulses preferentially stimulate portal osmoreceptors to cause the release of vasopressin, and suggest that portal osmoreceptors may be involved in the dynamic regulation of plasma osmolality.
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PMID:Vasopressin responses to peripheral and central osmotic pulse stimulation. 383 14

Mean arterial pressure, heart rate, plasma catecholamines, renin activity, and vasopressin changes induced by a 30-degree head-up tilt were studied before and during epidural anesthesia with bupivacaine in eight elderly patients (ages 58-82 yr). The tilt performed before epidural anesthesia did not modify mean arterial pressure, heart rate, plasma catecholamines, renin activity, and vasopressin at 5 and 15 min. During epidural anesthesia, the superior level of analgesia ranged from T4 to T10. Epidural anesthesia induced significant (P less than 0.05) decreases from control values in mean arterial pressure and plasma norepinephrine (from 85 +/- 6 to 67 +/- 8 mmHg and from 600 +/- 108 to 307 +/- 77 pg/ml, respectively, mean +/- SEM) without significant changes in heart rate, plasma epinephrine, renin activity, and vasopressin. However 5 and 15 min after tilt, significant decreases from pretilt values were measured in mean arterial pressure (from 67 +/- 8 to 57 +/- 6 and 55 +/- 6 mmHg, respectively) and in heart rate (from 70 +/- 8 to 63 +/- 7 and 62 +/- 7 beats/min). Simultaneously, an increase in plasma vasopressin (from 14.8 +/- 5.5 to 36.2 +/- 10.3 and 40.0 +/- 10.5 pg/ml) was recorded, whereas plasma norepinephrine and epinephrine remained unchanged. Posttilt plasma renin activity values at 5 and 15 min were increased significantly when compared with the preepidural values (2,752 +/- 1,168, 2,410 +/- 1,214 and 713 +/- 190 pg X ml-1 X h-1, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of epidural anesthesia on catecholamines, renin activity, and vasopressin changes induced by tilt in elderly men. 388 49

To elucidate the effect of bed rest used as an adjunct to increased diuretic treatment, twelve patients with chronic congestive heart failure (CHF) had a 50% increase in loop diuretic dosage and were allocated to either continuous bed rest or bed rest during nights only. The 24-hour bed rest group reduced their weight significantly (mean +/- SEM: 2.00 +/- 0.79 kg, P less than 0.001), whereas the night bed rest group had no significant weight reduction (1.10 +/- 0.37 kg, 0.1 less than P less than 0.2) during three days of observation. Furthermore, the 24-hour bed rest group had a significantly increased diuresis (P less than 0.05) during the first day of the study and a tendency towards increased natriuresis. The cumulated diuresis for the two groups (24-hour bed rest versus night bed rest) during the three days of study were 7773 +/- 700 ml and 5861 +/- 909 ml (0.05 less than P less than 0.1), respectively. Plasma concentrations of adrenaline, noradrenaline, renin and aldosterone were increased, as measured in the supine position. No significant differences were found between the two groups. Plasma concentrations of antidiuretic hormone were within normal limits. In conclusion, continuous bed rest is a reasonable adjunct to diuretic treatment in patients with CHF.
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PMID:Bed rest and increased diuretic treatment in chronic congestive heart failure. 391 4

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.
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PMID:Cerebrospinal fluid and plasma vasopressin in the fetal lamb: basal concentration and the effect of hypoxia. 396 53


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