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)

We hypothesize that hemodilution in the early stages of water immersion plays an important role in vasopressin (AVP) suppression and subsequent diuresis. Ten men (19-24 years) were immersed to the neck in a semireclining position for 8 h in 34.6 degree C tap water. After 8 h of immersion there were decreases (p less than 0.05) in plasma volume (PV) of 15.6%, extracellular volume (ECV) of 18.8%, interstitial volume (ISV) of 19.6%, and red cell volume of 10.7%. Hemodilution (hyposmotem years) were immersed to the neck in a semireclining position for 8 h in 34.6 degree C tap water. After 8 h of immersion there were decreases (p less than 0.05) in plasma volume (PV) of 15.6%, extracellular volume (ECV) of 18.8%, interstitial volume (ISV) of 19.6%, and red cell volume of 10.7%. Hemodilution (hyposmotem years) were immersed to the neck in a semireclining position for 8 h in 34.6 degree C tap water. After 8 h of immersion there were decreases (p less than 0.05) in plasma volume (PV) of 15.6%, extracellular volume (ECV) of 18.8%, interstitial volume (ISV) of 19.6%, and red cell volume of 10.7%. Hemodilution (hyposmotem of 4 mosmol/kg H2O) and near maximal suppression of AVP (to 0.5 pg/ml) and plasma renin activity (to 0.4 ng Ang 1 .ml-1.h-1) were evident by hour 2 of immersion. The early hemodilution (2-2 h) was due to a slight increase in PV with no change in plasma Na+ or osmotic content, even though urine volume and UosmV increased significantly. The hyposmotemia and PRA suppression continued throughout immersion in spite of the progressively increasing diuresis and decreasing PV. These findings suggest the transfer of hypotonic fluid into the vascular system; this fluid does not appear to come from the intracellular volume. We conclude that hyposmotemia is an important part of the mechanism contributing to AVP suppression during water immersion.
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PMID:Hemodilution, vasopressin suppression, and diuresis during water immersion in man. 725 90

Earlier observations that food restriction for a short period of time in the morning produced an altered circadian rhythm of plasma corticosterone having the peak just before feeding time, and that the elevated plasma corticosterone levels declined promptly immediately after food presentation were confirmed. After a 14-day restricted feeding schedule, where food was given from 11:00 to 13:00, if food was not given, elevated levels of plasma corticosterone were sustained for at least 1 hr and then declined gradually. On the other hand, if food was given 2 hr earlier than the scheduled time, the peak at 11:00 disappeared. The conditioned peak of plasma corticosterone was maintained for at least 3 days after the restricted feeding schedule if hypertonic saline, but not tap water, was given without food in male rats and ovariectomized female ones. When female rats were treated with lysine vasopressin for 5 days 10 min before the food presentation, highly elevated levels of plasma corticosterone were found at the time of food presentation. However, administration of cortisol 2 hr before the feeding time blocked the effect of vasopressin. The results suggest that vasopressin is involved in the acquisition and consolidation of the conditioned circadian rhythm of plasma corticosterone induced by restricted feeding.
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PMID:Conditioned circadian rhythm of plasma corticosterone in the rat induced by food restriction. 742 Jul 74

To determine which ovarian hormone is involved in the sexually dimorphic antidiuretic action of vasopressin, the antidiuretic response to vasopressin was examined in sham-operated nonestrous female rats chronically treated with vehicle and in ovariectomized rats treated with vehicle, progesterone, estradiol, or the combination of estradiol and progesterone, respectively. Three-week-old female rats were sham operated or ovariectomized, and a slow-release hormone pellet was implanted at the 6th wk. The experiment was performed at the 10th to 12th wk in conscious, chronically instrumented rats hydrated with tap water (2% body wt). Infusion of vasopressin at rates of 10-1,000 pg.min-1.kg body wt-1 resulted in a dose-dependent antidiuretic response that was significantly enhanced in ovariectomized rats compared with the intact nonestrous females. Progesterone had no effect, whereas estradiol attenuated and restored the antidiuretic response to vasopressin to a level similar to that in intact nonestrous female rats. These results suggest that it is estrogen, but not progesterone, that reduces the antidiuretic response to vasopressin in the female rat.
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PMID:Estradiol attenuates the antidiuretic action of vasopressin in ovariectomized rats. 773 6

The effect of hypertonic NaCl consumption on vasopressin (VP) and oxytocin (OT) mRNA levels and plasma and pituitary peptides was evaluated in rats with sham or anterior ventral third ventricular (AV3V) lesions. Rats were given tap water or 2% NaCl for 4 days. Because the rats with lesions drank significantly less salt solution than the controls (78.8 +/- 17.4 vs. 205.5 +/- 37.8 ml/4 days), a second control group was included in which saline intake was matched to the lesioned group. AV3V rats showed a deficit in the peptide response to the osmotic stimulus. There was no increase in plasma VP or OT or decrease in posterior pituitary peptide content in the face of an extreme hypernatremia: plasma sodium of 180.1 +/- 4.2 meq/l. Evaluation of mRNA changes by means of in situ hybridization showed that animals with lesions responded to the salt challenge with increases in hypothalamic VP and OT mRNA levels. There were significant increases in paraventricular and supraoptic OT mRNA and paraventricular VP mRNA in the lesioned group. The salt-matched control group showed no changes in peptide mRNA levels. These results demonstrate that AV3V lesions produce an impairment of the salt-neuroendocrine reflex but a persistence of the peptide mRNA response. Differences in control mechanisms must account for this dissociation between peptide mRNA expression and peptide secretion.
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PMID:Dissociation between vasopressin and oxytocin mRNA and peptide secretion after AV3V lesions. 781 Jul 75

Fetal urine flow is influenced by fetal intravascular volume, glomerular filtration rate, tubular reabsorption, and fluid regulatory hormones. As maternal-to-fetal fluid transfer is dependent on hydrostatic and osmotic gradients, we postulated that a chronic decrease in maternal plasma osmolality would promote transplacental fluid transfer and increase fetal urine flow. Six pregnant ewes and singleton fetuses (131 +/- 2 days; term = 150 days) received bladder and hindlimb arterial and venous catheters. After 5 days, plasma and urine composition, urine flow rate (Uvol), and plasma arginine vasopressin (AVP) levels were measured during a 2-h control period. At 2 h, tap water (2 liter, 38 degrees C) was administered to the ewe. At 3 h, ewes received a 20-micrograms bolus of 1-desamino-[D-Arg8]vasopressin (DDAVP), followed by continuous infusion (4 micrograms/h). In response to water loading, maternal urine osmolality decreased (761 +/- 158 to 339 +/- 13 mosmol/kgH2O), and Uvol increased. After DDAVP, maternal urine osmolality increased (1,270 +/- 89 mosmol/kgH2O), and Uvol, hematocrit, plasma osmolality (304 +/- 1 to 284 +/- 4 mosmol/kgH2O), and protein concentration decreased. Five hours after maternal DDAVP infusion, fetal plasma osmolality decreased (300 +/- 1 to 281 +/- 3 mosmol/kgH2O), and Uvol increased (0.4 +/- 0.1 to 1.3 +/- 0.2 ml/min) and remained elevated at 24 h. There was no change in fetal plasma DDAVP (immunoreactive AVP) levels or fetal urine osmolality. Controlled changes in maternal plasma osmolality may prove useful in modulating fetal urine flow and, ultimately, amniotic fluid volume.
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PMID:DDAVP-induced maternal hyposmolality increases ovine fetal urine flow. 786 29

Rats drinking ad libitum tap water or hypertonic (i.e. 2%) sodium chloride solution were given intracerebroventricularly (i.c.v.) for three days, thyrotropin-releasing hormone (TRH) in a daily dose of 200 ng dissolved in 10 microliters of 0.9% sodium chloride. Treatment with TRH resulted in significantly increased hypothalamic vasopressin content in both euhydrated (i.e. given tap water ad libitum) and salt-loaded rats. In rats given hypertonic saline, neurohypophysial vasopressin content increased. Plasma vasopressin concentration was distinctly diminished under TRH treatment, the respective difference being significant, however, barely in salt-loaded rats. The present data suggest that TRH may be involved in some regulatory processes related to vasopressin biosynthesis and release from the rat hypothalamo-neurohypophysial system.
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PMID:Thyrotropin-releasing hormone (TRH) inhibits vasopressin release from hypothalamo-neurohypophysial system of rats drinking hypertonic saline. 800 5

We profiled the concentrations of angiotensin I (Ang I), angiotensin II (Ang II), and angiotensin(1-7) [Ang(1-7)] by the combination of radioimmunoassay and high performance liquid chromatography in the blood of 14-week-old male Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR) drinking either tap water or a solution containing ceranapril (30 mg/kg) or lisinopril (20 mg/kg) for 14 days. Differences in the chemical and pharmacokinetic properties of the two converting enzyme inhibitors ruled out class-related effects. Plasma renin activity, angiotensin converting enzyme (ACE) activity, and plasma levels of Ang I and Ang II were the same in vehicle-treated WKY and SHR. In contrast, plasma levels of both Ang(1-7) and vasopressin in SHR were 3.7-fold and 2.6-fold higher, respectively (p < 0.05). Angiotensin converting enzyme inhibition reduced the blood pressure of WKY and SHR, and augmented their intake of water and output of urine. These changes were associated with increases in renin activity and plasma levels of Ang I and Ang(1-7). In both WKY and SHR, lisinopril had a greater effect in inhibiting plasma and cerebrospinal fluid ACE, reducing levels of plasma angiotensinogen, and increasing the concentrations of authentic Ang II. The principal finding of this study is that plasma Ang(1-7) is the sole component of the circulating angiotensin system that is elevated in the established phase of genetic hypertension. The finding that chronic inhibition of ACE augments circulating levels of Ang(1-7) evidenced the existence of functional pathways for the alternate processing of Ang I.
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PMID:Angiotensin(1-7) in the spontaneously hypertensive rat. 828 65

Rats drinking and libitum tap water or hypertonic (i.e., 2%) sodium chloride solution were given intracerebroventricularly (i.c.v.), during three days, thyrotropin-releasing hormone (TRH) in a daily dose of 200 ng dissolved in 10 microliters of 0.9% sodium chloride. Treatment with TRH resulted in significantly increased hypothalamic oxytocin content in both euhydrated (i.e., given tap water ad libitum) and salt-loaded rats and vasopressin content only in euhydrated rats. Similarly, neurohypophysial vasopressin and oxytocin content significantly increased in animals drinking tap water or 2% sodium chloride during treatment with TRH. The present data suggest that TRH may be involved in some regulatory processes to vasopressin and oxytocin biosynthesis and release from the rat hypothalamo-neurohypophysial system.
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PMID:Influence of thyroliberin (TRH) on hypothalamo-neurohypophysial vasopressin and oxytocin content of rats drinking 2% NaCl. 830 34

Ultrastructural studies of the supraoptic nucleus (SON) of the hypothalamus suggest that an active retraction and extension of astrocytic processes (structural plasticity) from between magnocellular neuroendocrine neurons plays a role in the release of oxytocin, vasopressin, or both peptides that accompanies parturition, lactation, and dehydration. In support of this, Salm et al. (1985) previously demonstrated a lactation-associated reduction in immunoreactive glial fibrillary acidic protein (GFAP), an astrocyte-specific cytoskeletal constituent. To determine if similar changes occur in response to dehydration, and if they are reversible, the present study examined GFAP-immunoreactivity (IR) in the SON under various hydration states. Rats were dehydrated for 7 days by substitution of drinking water with 2% saline (n = 3), or dehydrated for 7 days followed by 7 days of rehydration (n = 3). A control group (n = 3) with free access to tap water was used for comparisons. The optical density of GFAP-IR was obtained from the SON, globus pallidus, and lateral hypothalamic regions. The areas of the ventral glial limitans subjacent to the SON (SON-VGL) and of linearly equivalent segments of glial limitans more distant from the SON were also determined. Dehydration resulted in a significant reduction in GFAP-IR in the SON compared to control and rehydrated levels. We also found that the area of the SON-VGL was significantly larger than that of linearly equivalent segments of glial limitans elsewhere and that it was significantly reduced in dehydrated rats, returning to control levels with rehydration. GFAP-IR and glial limitans thickness in regions unrelated to body fluid homeostasis lateral to the SON, overlying to dorsal cortex, and subjacent to the optic chiasm were not significantly changed by hydration state. These results are similar to the changes of GFAP-IR reported for lactating rats and provide further evidence for a role of structural plasticity of astrocytes in events surrounding the selective functional activation of local neurons.
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PMID:Dehydration and rehydration selectively and reversibly alter glial fibrillary acidic protein immunoreactivity in the rat supraoptic nucleus and subjacent glial limitans. 948 12

The presence of corticotropin-releasing hormone (CRH) receptors type-1 (CRHR-1) and type-2 (CRHR-2alpha) in the hypothalamic supraoptic (SON) and paraventricular (PVN) nuclei, and the effects of i.c.v. injection of CRH and urocortin on arginine vasopressin (AVP) and oxytocin release, have suggested that CRH ligands have a role in osmoregulation. In this study, double labelling in situ hybridization using 35S-labelled CRHR-1 or CRHR-2alpha and digoxigenin-labelled AVP, oxytocin or CRH riboprobes was employed to examine the localization of CRHR-1 or CRHR-2alpha mRNA in the SON and PVN of control and osmotically stimulated rats. Rats received an i.p. hypertonic saline (1.5 M) injection or isotonic saline injection (controls), or 2% NaCl intake (salt loading) or tap water (controls) for 12 days. While CRHR-1 mRNA was undetectable in the SON and PVN in control rats, its expression was increased markedly at 4 h after i.p. hypertonic saline injection or after 12 days salt loading. Of the cells labelled with digoxigenin-AVP, 53% in the SON and 90% in the PVN coexpressed CRHR-1 mRNA after i.p. hypertonic saline injection. In oxytocinergic neurones, 73% in the SON and 91% in the PVN showed CRHR-1 autoradiographic grains higher than background levels after i.p. hypertonic saline injection. In addition, i.p. hypertonic saline induced CRHR-1 mRNA expression in digoxigenin-CRH stained cells in the parvocellular PVN. CRHR-2alpha transcripts were present in both the SON and PVN under basal conditions, and salt loading, but not acute i.p. hypertonic saline injection, further stimulated this expression. Double labelling in situ hybridization showed colocalization of CRHR-2alpha mRNA with AVP and oxytocin mRNA in the SON. These studies support a role for CRH and urocortin regulating the hypothalamo-neurohypophyseal system, and suggest a direct action of the peptides in the magnocellular neurones.
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PMID:Vasopressin and oxytocin neurones of hypothalamic supraoptic and paraventricular nuclei co-express mRNA for Type-1 and Type-2 corticotropin-releasing hormone receptors. 1097 8


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