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)

Studies were conducted to compare the metabolic effects of vasopressin, 4 beta-phorbol-12-myristate-13-acetate (PMA) and A23187 on ketogenesis and oleate metabolism in isolated hepatocytes from fed rats. Vasopressin inhibited the formation of acid-soluble products from [1-14C]oleate (0.25 mM, 0.5 mM and 1 mM), the inhibition being most marked at low (0.25 mM) concentration of oleate. Conversion of [1-14C]oleate into 14CO2 and esterified products was stimulated by vasopressin. The stimulatory effect of this hormone on 14CO2 production was most marked at high (1 mM) concentration of oleate, whereas that on [1-14C]oleate esterification was most marked at low (0.25 mM) concentration of oleate. These vasopressin actions were abolished when hepatocytes were incubated in the absence of calcium in the medium. Our results strongly suggest that both increase in esterification and increase in oxidation to CO2 contribute to the anti-ketogenic action of vasopressin when oleate is added as substrate, although the relative extent of their contribution varies according to the oleate concentration. The anti-ketogenic action of vasopressin was mimicked by PMA but not by A23187. PMA also caused a stimulation of [1-14C]oleate esterification although the effect was diminished at 1 mM [1-14C]oleate. A23187 failed to affect [1-14C]oleate esterification. The metabolic effects of PMA were elicited in the absence of extracellular calcium, too. Conversion of [1-14C]oleate into 14CO2 was only slightly increased by both PMA and A23187 when 1 mM [1-14C]oleate was added as substrate. The marked stimulatory effect of vasopressin on 14CO2 production from [1-14C]oleate was not reproduced even by the combination of PMA and A23187.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of phorbol esters, A23187 and vasopressin on oleate metabolism in isolated rat hepatocytes. 311 84

Neurohypophysial blood flow responses to hypoxic hypoxia were studied under conditions of vagotomy, carotid sinus denervation, and combined vagotomy and carotid sinus denervation. Arterial O2 tension was lowered from 128 +/- 3 to 31 +/- 1 Torr, whereas pH and arterial CO2 tension remained constant. Denervation of either carotid sinus or aortic arch chemoreceptors alone does not attenuate the dilation of neurohypophysial vessels that accompanies hypoxic hypoxia. Combined denervation, however, completely blocks this response for the neurohypophysis but not for any other brain region studied. Hypoxic hypoxia resulted in an increase in plasma vasopressin (AVP) from approximately 8 to approximately 40 pg/ml. This increase occurred in the intact, vagotomy, and carotid sinus-denervation conditions. This neurosecretory response was also completely inhibited by combined denervation. For most brain regions peripheral chemoreceptors are not involved in the blood flow response; however, the response of the neurohypophysis appears to be mediated via these chemoreceptors, presumably by altering the neuroeffector activity to this region. In addition our data suggest a temporal relationship between neurohypophysial vasodilation and neurosecretion of AVP.
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PMID:Peripheral chemoreceptor control of neurohypophysial blood flow. 312 21

Differential interference contrast microscopy was used in combination with standard electrophysiological techniques in the in vitro perfused mouse medullary thick ascending limb of Henle's loop (MAL) to evaluate the cell volume responses of this nephron segment during and following exposure to hypotonic media and to assess the role of antidiuretic hormone (ADH) and net salt absorption on the associated volume regulatory processes. Reductions in extracellular osmolality by 50 mosmol resulted in rapid increases in cell volume of approximately 20% with or without exposure to ADH. Cell volume recovery (volume-regulatory decrease, VRD) was much slower in the presence, than in the absence, of ADH. This hormone-mediated impairment of the VRD response could be overcome by the abolishment of net salt absorption with luminal 10(-4) M furosemide. An inverse linear relationship was observed between the rates of net salt absorption and VRD, indicating a finite ability of this nephron segment to enhance solute exit mechanisms whether induced by increases in transcellular traffic or by hypotonic cell swelling. Finally, returning to the isotonic media resulted in cell shrinkage under all conditions [+/- ADH and +(ADH and furosemide)] consistent with cell solute loss mediating VRD. However, recovery of cell volume back to the initial isotonic control value [post-VRD volume regulatory increase (VRI)] was only observed in ADH-treated tubules and was independent of net salt absorption. The post-VRD VRI response could be abolished by isohydric CO2-HCO3- removal or by addition of 10(-4) M amiloride to the peritubular medium. The latter results suggest that parallel Na+-H+ and Cl- -HCO3- exchangers located in basolateral membranes mediate the post-VRD VRI response.
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PMID:Hypotonic cell volume regulation in mouse medullary thick ascending limb: effects of ADH. 314 72

Vasopressin and oxytocin exert pronounced effects on behaviour by a direct action on the brain. A single injection of vasopressin results in a long-term inhibition of extinction of a conditioned avoidance response suggesting that vasopressin triggers a long-term effect on the maintenance of a learned response, probably by facilitation of memory processes. In addition vasopressin improves passive avoidance behaviour, delays extinction of appetitive discrimination tasks, affects approach behaviour to an imprinting stimulus in ducklings, improves copulation rewarded behaviour of male rats in a T-maze, prevents or reverses amnesia induced by electroconvulsive shock, CO2 inhalation, pentylenetetrazol or puromycin. The majority of these effects of vasopressin in the various and sometimes relatively complex tasks may be explained by stimulatory influences of this neuropeptide on memory processes. Generally oxytocin exerts effects which are opposite to those of vasopressin and it has been suggested that oxytocin may be an amnesic neuropeptide. Various limbic system structures seem to act as the anatomical substrate for the behavioural effects of vasopressin. In particular the amygdala, the dentate gyrus of the hippocampal complex, the ventral hippocampus and the dorsal septum seem to be involved. Evidence has been obtained from experiments with homozygous diabetes insipidus rats and from experiments in which antisera were applied that endogenous vasopressin and oxytocin play a physiological role in brain processes related to memory. It appears that highly active fragments can be generated from vasopressin and experiments in which a fragment of vasopressin ([pGlu4, Cyt6]AVP-(4-8)) as well as an AVP-antagonist were used, reveal that the vasopressin receptors mediating the behavioural effects are situated in the brain and differ in specificity from the peripheral (blood pressure) vasopressin receptors. Generally the clinical data obtained so far with vasopressin treatment are in agreement with the results from animal experiments and they support the notion on the involvement of vasopressin in memory function. The sometimes reported conflicting results on vasopressin effects in certain patients (Korsakoff or Alzheimer) may have to do with the wide-spread pathology in these diseases.
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PMID:Vasopressin and oxytocin. Their presence in the central nervous system and their functional significance in brain processes related to behaviour and memory. 346 10

The nature of the activity of vasopressin which is responsible for the inhibition of renin secretion was studied by comparing the effects of vasopressin (AVP) and analogs of AVP in anesthetized water-loaded dogs. Infusion of AVP (1.0 ng/kg/min) increased mean arterial pressure (MAP) and decreased heart rate (HR) and free water clearance (CH2O). Plasma renin activity (PRA) decreased from 11.9 +/- 4.7 to 3.8 +/- 1.7 ng/ml/3 hr (p less than 0.05). A selective antidiuretic agonist, 1-deamino-8-D-arginine vasopressin (1.0 ng/kg/min), which had no effect on MAP or HR but was effective as AVP in decreasing CH2O, decreased PRA from 13.5 +/- 4.6 to 7.0 +/- 2.9 ng/ml/3 hr (p less than 0.05). Infusion of a selective vasoconstrictor agonist, 2-phenylalanine-8-ornithine oxytocin (1.0 ng/kg/min), increased MAP and decreased HR but did not decrease CH2O or PRA. A vasoconstrictor antagonist, d(CH2)5Tyr(Me)AVP (10 micrograms/kg), completely blocked the MAP and HR responses to AVP but did not block the decrease in CH2O or PRA (5.9 +/- 1.8 to 2.9 +/- 1.6 ng/ml/3 hr) (p less than 0.001). Infusion of the 0.45% saline vehicle had no significant effect on MAP, HR, CH2O or PRA. These results indicate that the inhibition of renin secretion by vasopressin in anesthetized water-loaded dogs is due to its antidiuretic activity.
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PMID:Role of antidiuretic activity in the inhibition of renin secretion by vasopressin in anesthetized dogs. 352 May 11

Decreased urinary output (Vu ml/min) after institution of PEEP is attributed to a variety of mechanisms including decreased cardiac output and renal blood flow (RBF), activation of neurohormonal reflexes, increased catecholamines, plasma renin activity (PRA), and antidiuretic hormone (ADH) release. To evaluate these factors, seven normovolemic patients (36 yr +/- 13 SD), free of preexisting lung, cardiac, or renal disease, requiring continuous mandatory ventilation for neurologic reasons were studied. The authors measured or calculated: total blood volume (TBV) (51Cr); right atrial, pulmonary arterial, pulmonary wedge, and systemic pressures, cardiac index (CI); renal plasma flow (RPF) (iodohippurate sodium 131I [131I PAH] clearance); glomerular filtration rate (GFR) (creatinine clearance), free water clearance (CH2O), osmolal clearance (Cosm), fractional excretion of sodium (FENa+) and potassium (FEK+); and plasma renin activity (PRA) (ng X ml-1 X h-1), plasma ADH (pg/ml; radioimmunoassay), epinephrine (E in pg/ml), and norepinephrine (NE in pg/ml) (double-isotope radioenzymatic assay). Two conditions were studied after 90-min steady state: 1) zero PEEP (ZEEP); and 2) 15 cmH2O PEEP. PEEP caused a significant decrease in CI (-21%; P less than 0.01) and RPF (-19%; P less than 0.05) without significant decrease in GFR. A significant decrease in Vu (-55%; P less than 0.05), FENa+ (-39%; P less than 0.05) and Cosm (-36%; P less than 0.25) occurred without modification in CH2O. Plasma ADH remained in the normal range and did not increase when PEEP was applied.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:No involvement of antidiuretic hormone in acute antidiuresis during PEEP ventilation in humans. 354 90

Paired micropuncture experiments were carried out in plasma-replete volume-expanded rats to examine the acute effects of 1-desamino-8-D-arginine vasopressin (dDAVP) on urinary acidification and tubular handling of bicarbonate and chloride. No effect was detected on the fractional absorption of water, total CO2, and chloride at end-proximal and early distal sites of superficial nephrons in intact animals; dDAVP, however, inhibited the fractional absorption of total CO2 in Henle's loop while stimulating that of chloride in thyroparathyroidectomized (TPTX) somatostatin-infused rats. In the distal tubule accessible to micropuncture, net total CO2 secretion was observed during hypotonic volume expansion, which reversed to net total CO2 absorption during dDAVP infusion in intact Wistar rats. Marked stimulation of urinary acidification occurred in all animals as attested by a fall in urine pH and bicarbonate excretion. Net acid excretion almost doubled in intact rats. We conclude that (a) antidiuretic hormone (ADH) inhibits fractional bicarbonate absorption in the thick ascending limb while stimulating that of chloride at least in TPTX somatostatin-infused rats, and (b) ADH stimulates proton secretion (or inhibits bicarbonate secretion) in the distal tubule and cortical collecting ducts, which leads to enhanced urinary acidification.
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PMID:Effects of antidiuretic hormone on urinary acidification and on tubular handling of bicarbonate in the rat. 362 81

Neurohypophyseal blood flow was studied using radiolabelled microspheres in 13 dogs. Hypoxic hypoxia and carbon monoxide hypoxia with similar arterial oxygen contents (CaO2, approximately 8 vol %) were produced. Under conditions of hypoxic hypoxia, 100-200% increases in blood flow in caudate nucleus, white matter, neurohypophysis, and all other brain regions occurred. Similar blood flow responses were observed with carbon monoxide hypoxia in all brain regions except the neurohypophysis. The role of carotid and aortic chemoreceptors in mediating this blood flow response was studied in 6 additional dogs. Similar degrees of hypoxic hypoxia were produced in chemoreceptor-intact and completely denervated animals (CaO2 approximately 8 vol %, PaO2 approximately 33 mm Hg). Hypoxic hypoxia produced a 250% increase in neurohypophyseal blood flow and a concurrent rise in plasma arginine vasopressin from 8 +/- 3 to 52 +/- 8 pg/ml. Chemoreceptor denervation completely inhibited the increase in neurohypophyseal blood flow associated with hypoxic hypoxia. Arginine vasopressin was not increased by hypoxic hypoxia under conditions of complete denervation. A unique role for peripheral chemoreceptors in regulating neurohypophyseal blood flow is postulated.
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PMID:Influence of chemoreceptors on neurohypophyseal blood flow during hypoxic hypoxia. 366 88

We examined the renal effects of synthetic oxytocin (OT) in the presence and absence of vasopressin in conscious euvolemic rats. Both sexes of the Long-Evans (LE) and Brattleboro homozygous (DI) strains were used. OT infused intravenously at 0.25 and 2.5 ng X min-1 X 100 g body wt (BW)-1 resulted, respectively, in plasma concentrations of 30 +/- 6 and 265 +/- 88 pg/ml in LE rats and 46 +/- 5 and 327 +/- 29 pg/ml in DI rats. Glomerular filtration rate (GFR) was augmented most consistently by the larger dose of hormone in LE rats (P less than 0.05), whereas the low infusion rate of OT enhanced GFR in DI rats (P less than 0.01). Effective renal plasma flow was not changed significantly. OT (both doses) increased the fractional excretion of sodium two- to threefold in each strain of animal (all at least P less than 0.05 from control), whereas the fractional excretion of potassium was largely unaffected. In LE rats, a diuresis was observed with either infusion rate of hormone, accompanied by a rise in osmolar clearance (COsm). In contrast, there was no change of urine flow with the low dose of OT in DI rats, because COsm increased and the clearance of free water (CH2O) decreased proportionately. The higher infusion rate of OT promoted antidiuresis in DI rats, with negative CH2O and little change in COsm. We conclude that oxytocin enhances GFR and is natriuretic regardless of the presence or absence of endogenous vasopressin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of oxytocin on renal hemodynamics and electrolyte and water excretion. 374 Feb 76

Sudden unexplained death may be seen with treatment of craniovertebral anomalies and surgery of the upper cervical spine. Death is due to sleep-induced apnea, premonitored by periods of confusion, lethargy, and asthenia. There may be associated hypotension, bradycardia, hyponatremia, hypothermia, inappropriate antidiuretic hormone secretion, and difficulty in micturition. The potential for respiratory failure may be predicted if a CO2 response test demonstrates an attenuated or abnormal response. Apnea during sleep may be reversed by arousal or may require ventilatory support for a period of time. The condition is self-limiting, but remains the major life-threatening complication. Both apnea and autonomic dysfunction are treatable and curable with appropriate diagnosis and management.
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PMID:Occult respiratory and autonomic dysfunction in craniovertebral anomalies and upper cervical spinal disease. 375 66


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