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)

Four open, dry Holstein cows in the University of Missouri Climatic Laboratory were used to study the effect of adrenocorticotropic hormone administration on glucocorticoids and antidiuretic hormone of plasma in two reversal trials at thermoneutral (20 C, 50% relative humidity) and heat (33 C, 50% relative humidity) conditions. Average glucocorticoids (saline versus adrenocorticotropic hormone) at thermoneutral were 8.3 and 41.2 ng/ml while values for heat were 6.2 and 40.4 ng/ml. The effect of heat on glucocorticoids of plasma was not significant. Injection of adrenocorticotropic hormone under thermoneutrality and heat caused a marked increase in antidiuretic hormone within 5 min which lasted to 120 min. At thermoneutral average antidiuretic hormone levels (saline versus adrenocorticotropic hormone) were .5 and 1.9 pg/ml while values for heat were 1.8 and 3.6 pg/ml. Antidiuretic hormone concentrations under heat were higher than thermoneutral in cows injected with saline and andrenocorticotropic hormone. The fast response of antidiuretic hormone of plasma to exogenous adrenocorticotropic hormone suggests that adrenocorticotropic hormone might act directly at higher levels of the central nervous system causing release of antidiuretic hormone.
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PMID:Effect of adrenocorticotropic hormone on plasma glucocorticoids and antidiuretic hormone of cattle exposed to 20 and 33 C. 20 64

1. Recordings were made from a total of 35 antidromically identified neurones in the paraventricular (PV) and supraoptic (SO) nuclei of urethane-anaesthetized lactating rats. During recording plasma osmotic pressure was raised by 12 m-osmole/kg by injection of hypertonic solutions of NaCl, LiCl, or mannitol.2. Nine PV neurones (mean firing rate 4.2 +/- 1.0 (S.E.) spikes/sec) were classified as oxytocin cells because they gave a burst of activity before reflex milk-ejections. None of these showed a bursting (phasic) firing pattern. Ten PV neurones (mean firing rate 1.8 +/- 0.2 spikes/sec) fired phasically either before or after injection of hypertonic NaCl and were classified as vasopressin cells. The remaining six PV cells (mean firing rate 1.6 +/- 0.9 spikes/sec) showed no bursts of firing related to milk ejection and did not fire phasically.3. Increasing plasma osmotic pressure by injection of hypertonic NaCl increased the mean firing rate of PV oxytocin cells to 7.0 +/- 1.0 spikes/sec. Vasopressin cells in the PV nucleus were much less responsive and the mean firing rate after injection was 2.9 +/- 0.4 spikes/sec. The third group of PV neurones was unresponsive.4. Plasma oxytocin concentration (determined by radioimmunoassay) increased from 2.1 +/- 0.3 muu./ml. in the control period to 10.9 +/- 2.8 muu./ml. 30 min after I.P. injection of 1 ml. 1.5 M-NaCl and to 14.8 +/- 2.8 muu./ml. following injection of a second 1 ml. 1.5 M-NaCl.5. The responses of oxytocin and vasopressin neurones in the SO nucleus to an increase in plasma osmotic pressure following injections of hypertonic solutions of LiCl or mannitol were similar to those observed when plasma osmotic pressure was raised by NaCl.6. It may be concluded that both oxytocin and vasopressin cells in the neurohypophysical system are responsive to the osmotic pressure of the blood plasma rather than to Na(+) or Cl(-) concentration, that osmotic activation of oxytocin cells releases sufficient oxytocin to increase its plasma concentration, and that there may be a functional difference between the SO and PV nuclei.
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PMID:Oxytocin release following osmotic activation of oxytocin neurones in the paraventricular and supraoptic nuclei. 20 73

Current experimental evidence indicates that endogenous renal medullary prostaglandins modulate the antidiuretic response to vasopressin in the mammalian kidney. The predominant effect of prostaglandins is to attenuate the antidiuretic response to vasopressin; inhibition of prostaglandin synthesis potentiates the renal effect of vasopressin. Prostaglandins likely antagonize the renal effects of vasopressin at the cellular level of hormone-dependent cyclic adenosine 3,5-monophosphate metabolism, but the exact molecular mechanism is not known. Likewise, it is not known whether such modulatory effect is due to primary prostaglandins, prostaglandin precursors or to other metabolites of arachidonic acid. Vasopressin itself could stimulate intrarenal prostaglandin synthesis; this effect may represent a negative-feedback regulatory pathway for the antidiuretic response to the hormone. Recent experimental evidence suggests that modulatory effect of prostaglandin may be a factor in pathogenesis of some types of urinary concentrating defects.
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PMID:Cellular interactions between vasopressin and prostaglandins in the mammalian kidney. 21 51

Vasopressin increases the permeability of receptor cells to water and, in tissues such as toad bladder, to solutes such as urea. While cyclic AMP appears to play a major role in mediating the effects of vasopressin, there is evidence that activation of the water permeability system and the urea permeability system involves separate pathways. In the present study, we have shown that inhibitors of oxidative metabolism (rotenone, dinitrophenol, and methylene blue) selectively inhibit either vasopressin-stimulated water flow or vasopressin-stimulated urea transport. There was no inhibition, however, when exogenous cyclic AMP was substituted for vasopressin, and little to no inhibition when the potent analogue 8-bromoadenosine 3',5'-cyclic monophosphate (8-Br-cAMP) was employed. Rotenone had no effect on adenylate cyclase activity or cyclic AMP levels within the cell; dinitrophenol decreased adenylate cyclase activity minimally. Additional studies with vinblastine and nocodazole, inhibitors of microtubule assembly, demonstrated an inhibition of vasopressin and cyclic AMP-stimulated water flow but showed no effect on urea transport. We would conclude that water and urea transport, as examples of hormone-stimulated processes, have different links to cell metabolism, and that in addition to cyclic AMP, a non-nucleotide pathway may be involved in the action of vasopressin.
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PMID:Effect of metabolic inhibitors on vasopressin-stimulated transport systems in the toad bladder. 22 66

The effects of vasopressin and cyclic AMP on water transport at arachnoid villi into the superior sagittal sinus were examined using the isolated meninges preparations of cats. The meninges preparation, the superior sagittal sinus of which was opened at the midline of the outer surface, was held between two polyethylene tubes. The tubes were fixed vertically in the way that the opened surface of the sinus was directed downward and arachnoid surface upward. Water transport was determined by measuring the tritiated water dripping through the membrane preparation. Vasopressin from less than 50 to 500 muU/ml accelerated the water transport and this effect was dose-dependent. Cyclic AMP from 0.5 to 10 mM was proved to manifest the same effect as vasopressin. This effect of cyclic AMP appeared rapidly in comparison with that of vasopressin, suggesting that the effect of vasopressin may be manifested through cyclic AMP. From these findings a physiological role of vasopressin in cerebrospinal fluid was discussed regarding the regulation of intracranial pressure.
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PMID:Effects of vasopressin and cyclic AMP on water transport at arachnoid villi of cats. 22 64

Substance P stimulation of salivation in rats has been studied as has its in vitro enhancement of amylase release by isolated parotid cells. The extent of the stimulation on amylase release by isolated parotid cells was dependent upon the concentration of substance P, with the minimum effective concentration being 1 nM. The substance P effect was detectable within 1 min after incubation and lasted for at least 50 min. Substance P stimulation was demonstrable at 25--37 degrees C but not at 0 degrees C. Adrenocorticotropic hormone (ACTH), thyrotropin-releasing hormone (TRH), vasopressin and neurotensin had no effect on amylase release. These results suggest that substance P may act directly on the parotid cells. Examination of the salivary-stimulating activity of fragments of substance P showed that the C-terminal octapeptide and (pyroglutamyl)hexapeptide were active, although less potent than substance P, whereas its free acid, C-terminal tetra- and tri-peptides were inactive. Vasopressin, angiotensin II and neurotensin could inhibit substance P induced salivation, whereas TRH, ACTH and somatostatin had no effect. Amylase activity per unit volume of saliva was not changed by the injection of vasopressin, angiotensin II or neurotensin. These vasoactive peptides did not affect substance P stimulation of amylase release by isolated parotid cells. The results indicate that vasopressin, angiotensin II and neurotensin inhibit the action of substance P on salivation at sites other than the parotid cells.
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PMID:Substance P stimulation of amylase release by isolated parotid cells and inhibition of substance P induction of salivation by vasoactive peptides. 22 41

Aqueous vasopressin was infused to bicarbonate- and glucose-loaded dogs and to nonloaded antidiuretic dogs in doses of 50 mU/kg per min or 50 mU/kg per h. Both doses caused a marked increase in sodium, chloride, and water excretion. The larger dose raised the fractional excretion (sodium clearance (C-Na)/glomerular filtration rate (GFR) times 100) of these ions from 2% or less to in excess of 20%. Blocking the pressor effects of these doses of vasopressin with sodium nitroprusside did not alter the marked natriuretic and chloriuretic effect. The maximal rate of bicarbonate and glucose reabsorption was not depressed by vasopressin infusion; fractional phosphate excretion, however, was markedly increased. Inhibiting distal hydrogen ion secretion by inducing selective aldosterone deficiency failed to uncover a vasopressin-induced inhibition of proximal bicarbonate reabsorption that might have been masked by increased distal bicarbonate reabsorption. There was no significant change in GFR, renal plasma flow, or filtration fraction. The distribution of cortical renal blood flow (measured by the radioactive microsphere technique) shifted toward the inner cortex after vasopressin administration. Vasopressin, in pharmacologic doses, is a potent diuretic that most likely exerts this effect by directly inhibiting sodium reabsorption at a point in the nephron distal to the proximal tubule.
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PMID:Effect of infusion of pharmacologic amounts of vasopressin on renal electrolyte excretion. 23 93

Vasopressin and other neurohypophyseal peptides affect various processes related to memory and/or learning. A single subcutaneous injection of vasopressin increases resistance to extinction of a pole-jumping avoidance response in rat. This test system has been applied in an attempt to relate structural aspects of neurohypophyseal peptides, analogues, and derivatives with truncated sequences to their effects on conditioned behavior. Thus far it can be concluded that there are more stringent requirements on certain residues in the 20-member covalent ring than in positions 8 and 9 of the linear peptide portion for neurohypophyseal hormones to be active. Critical are the contributions of residues in positions 2, 3, and 5; these results are reminiscent of those from conformation-activity correlations of the endocrine effects of neurohypophyseal hormones, in which the side chain of the residue in position 3 is critical for receptor binding and the side chains of residues in positions 2 and 5 are key for the activation of the receptor. Chemical modifications in position 4 yield analogues that are active and inactive in increasing the resistance to extinction of the avoidance response, depending on the particular structural substitution, similar to results from structure-activity studies of the endocrine activities of neurohypophyseal hormones. Because behavioral activities of vasopressin are more tolerant than endocrine activities to modifications of the hormone in positions 8 and 9, analogues with the most striking dissociation of potencies in learned behavior and endocrine responses are expected to be those with sequence alterations in the linear peptide portion. Peptides with linear part sequences of neurohypophyseal hormones showed little or no activity. The results obtained in this structure-activity study are compared with those of an earlier study in which the ability of various neurohypophyseal peptides to attenuate puromycin-induced amnesia in mice was evaluated.
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PMID:Modification of conditioned behavior of rats by neurohypophyseal hormones and analogues. 27 85

1. The role of vasopressin in blood pressure control and in the pathogenesis of one-kidney Goldblatt hypertension in the conscious dog was investigated. 2. Infusion of synthetic arginine vasopressin to elevate plasma levels approximately five-fold caused bradycardia in normal dogs and increase in mean arterial blood pressure in dogs with pharmacological autonomic blockade. 3. A similar degree of elevation of plasma vasopressin concentration was observed after mild non-hypotensive haemorrhage. 4. Renal artery constriction in unilaterally-nephrectomized dogs caused a rise in plasma renin activity and only a doubling of plasma vasopressin concentration, but a marked rise in mean arterial blood pressure. 5. Vasopressin may play a role in normal cardiovascular homeostatic responses, but its role in the pathogenesis of this form of hypertension is unlikely to be significant.
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PMID:The role of vasopressin in blood pressure control and in experimental hypertension. 28 63

Transverse sections of the median eminence from fetal and neonatal rats were examined by the immunoperoxidase technique to detect the presence of oxytocin, vasopressin and neurophysin. Neurophysin was observed in the 18-day fetus. Vasopressin and oxytocin were not detected until after birth, on the 4th and 8th days respectively. There was an accumulation of material crossreactive with neurophysin and vasopressin antibodies in the palisade layer of the median eminence between the 4th and 9th days after birth. This distribution of immunoreactive material in the palisade layer was suggestive of neurosecretory substances localized in two fibre tracts on either side of the median eminence. The data are consistent with the accumulation of corticotropin releasing factor and an associated neurophysin in this area. It is suggested that the accumulation of material occurs because of the relative immaturity of the capillary loops that constitute the primary plexus of the hypophysial portal system.
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PMID:Maturation of the hypothalamo-neurohypophysial system. II. Neurophysin, vasopressin and oxytocin in the median eminence of the developing rat brain. 31 38


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