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)

In conscious rats, intracerebroventricular (i.c.v.) injections of gamma-aminobutyric acid (GABA), a GABA-uptake inhibitor (nipecotic acid), and artificial CSF (aCSF) were restricted to forebrain regions and their effect on baroreceptor-mediated arginine-vasopressin (AVP) release was studied. AVP release was stimulated by the hypotension resulting from combined treatment with a converting enzyme inhibitor (CEI) and chlorisondamine (CHLOR), a ganglionic blocking agent. CEI + CHLOR reduced mean arterial pressure (MAP) from 118 +/- 2 to 63 +/- 2 mm Hg, but pressure then rose to a compensated level of 78 +/- 1 mm Hg. The compensation in MAP was shown to be AVP-dependent at the end of the experiment since the vascular AVP antagonist, d(CH2)5Tyr(Me)AVP, reduced MAP from 78 +/- 1 to 63 +/- 1 mm Hg. While AVP was contributing to MAP maintenance, GABA (15, 50 and 150 micrograms) caused dose-related reductions in MAP (5 +/- 1.7 +/- 1 and 11 +/- 2 mm Hg, respectively). Nipecotic acid (3-350 micrograms) also caused dose-related reductions in MAP (from 3 +/- 1 to 15 +/- 2 mm Hg), while aCSF had no effect on MAP. Pretreatment with d(CH2)5Tyr(Me)AVP, antagonized completely the depressor effects of GABA and nipecotic acid. In other rats, blood samples were taken to measure the changes in plasma AVP concentrations (pAVP) induced by CEI + CHLOR and subsequent treatment with aCSF or nipecotic acid (175 micrograms). Hypotension induced by CEI + CHLOR caused a significant increase in pAVP. Forebrain-restricted nipecotic acid significantly suppressed pAVP (61 +/- 8% reduction; P less than 0.05 vs aCSF). These data provide evidence of an endogenous forebrain GABAergic system which, when activated, can inhibit baroreceptor-mediated AVP release.
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PMID:Evidence of an endogenous forebrain GABAergic system capable of inhibiting baroreceptor-mediated vasopressin release. 280 69

Arginine-vasopressin (AVP) levels and osmolality were measured in the CSF of rats during 5 days of osmotic stimulation. Dehydration increased AVP levels about 3-fold but did not affect the circadian rhythm of AVP. During dehydration, AVP levels in CSF increased as osmolality increased. Neither AVP levels nor osmolality changed significantly in the CSF of rats receiving 2% NaCl as drinking water. The increased AVP values in CSF may reflect activated release of AVP in the central nervous system during dehydration. Our data also suggest that the AVP release connected with the regulation of osmotic changes may be separate from the mechanism that regulates the circadian rhythm of AVP in the CSF of rats.
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PMID:Effects of osmotic stimuli on vasopressin levels in the CSF of rats. 285 36

CSF neurotransmitter markers may reflect neurochemical alterations in Alzheimer's disease (AD). The best studied neurochemical deficit in AD is that of acetylcholine. Both acetylcholinesterase and butyrylcholinesterase activity have been reported to be reduced in some but not all studies of AD CSF. Studies of monoamine metabolites have also been controversial but most authors have found reduced concentrations of CSF HVA, lesser reductions in HIAA and no change in MHPG. CSF GABA concentrations have been found to be reduced in AD. Studies of CSF neuropeptides in AD have shown reduced concentrations of somatostatin and vasopressin, normal concentrations of vasoactive intestinal polypeptide and either normal or decreased concentrations of beta-endorphin and corticotropin releasing factor. Although no individual CSF neurochemical markers are specific for AD it may be possible to develop a profile of several neurochemical markers which will have enhanced specificity.
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PMID:CSF neurotransmitter markers in Alzheimer's disease. 287 17

Levels of vasopressin, somatostatin, neurotensin, vasoactive intestinal peptide, corticotrophin-releasing factor and adrenocorticotrophin in CSF were determined in lithium-treated and unmedicated euthymic bipolar patients and controls, in a search for a trait marker in affective disorder. No group differences in levels of these peptides were found. Highly significant positive correlations were found among these peptides (with the exception of neurotensin), suggesting that their presence in CSF is functionally significant, as opposed to the result of random diffusion from the interstitial space of the brain.
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PMID:CSF neuropeptides in euthymic bipolar patients and controls. 288 3

Barrel rotation (BR) is an abnormal, long-axis rotation induced by intracerebroventricular (i.c.v.) injections of peptides, including somatostatin (SRIF) and arginine-vasopressin (AVP). This study examined the effects of two i.c.v. doses of SRIF and combined injections of SRIF and AVP in conscious, adult Wistar and Sprague-Dawley rats. Mortality after i.c.v. SRIF was dose-dependent; 0/16 rats died after a 20 microgram dose, while 21/43 died after 40 micrograms SRIF. On the other hand, BR incidence was similar after the two doses, but the hazard function of the BR latency data was shifted to the left by the higher dose. Although the incidence data imply that BR and mortality are independent, the hazard function of BR latency data is predictive of mortality. An interaction study employing a combined i.c.v. dose of 20 micrograms SRIF and 0.5 micrograms AVP established that the effects add non-linearly. This is illustrated by a marked increment in mortality (0/16 for 20 micrograms SRIF, 1/25 for 0.5 micrograms AVP and 12/18 for SRIF + AVP). The hazard plot shows a similar, non-linear interaction. In addition, SRIF, but not AVP, produced a characteristic pattern of Purkinje cell death in cerebellar regions projecting to the fastigial and lateral vestibular nuclei. These results imply that SRIF and AVP act at independent sites to produce BR and mortality, and that the effects summate non-linearly at a common central site. This raises the issue of whether these neuropeptides, endogenous in human CSF, interact to produce similar biological effects.
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PMID:Motor disturbances and neurotoxicity induced by centrally administered somatostatin and vasopressin in conscious rats: interactive effects of two neuropeptides. 289 27

The role of the brain opioid system in the control of hypothalamic-pituitary-adrenal activity was studied in 10 conscious sheep with an indwelling cannula in a cerebral lateral ventricle. On separate days, sheep received infusions of artificial CSF (control) and the opiate antagonist, naloxone (100 micrograms/hr) before and during acute moderate hemorrhage (15 ml/kg over 10 min). Infusion of naloxone before hemorrhage raised plasma ACTH and resulted in a significant increase in cortisol compared to the control infusion. In contrast, ACTH and cortisol responses to hemorrhage tended to be blunted by central naloxone infusion. The responses of vasopressin, aldosterone and the catecholamines remained unaffected by naloxone. The fall in blood pressure and the rise in heart rate accompanying hemorrhage were likewise unaltered. These results suggest that brain opioid peptides have an inhibitory effect on basal ACTH secretion but do not play a major role in modulating the hemodynamic or pituitary-adrenal responses to acute moderate hemorrhage in conscious sheep.
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PMID:Effect of central naloxone on hormone and blood pressure responses to hemorrhage in conscious sheep. 303 28

The acute administration of ANG II into the brain of experimental animals produces transient pressor effects, a marked increase in drinking, release of the antidiuretic hormone, increase in total peripheral resistance, a diuretic and natriuretic effect and an increase in sympathetic outflow. The chronic administration of ANG II into a cerebrolateral ventricle produces sustained pressor effects only if 0.9% sodium chloride solution is used as the drinking fluid. The hypertension is due to an increase in total peripheral resistance which appears to be due to an increase in intrinsic tone of vascular smooth muscle. In addition there was enhanced responsiveness of the vasculature to norepinephrine and ANG II and a decrease in reflex vasodilatation of the hind limb of ANG II treated dogs. The chronic elevation of ANG II in the CSF plus an increase in NaCl intake produces a low renin, sodium dependent, expanded volume hypertension. Data are presented suggesting that this model of hypertension is induced by the central release of an inhibitor of the Na+,K+-Pump.
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PMID:The central effects of the renin-angiotensin system. 328 Jan 70

The onset of therapeutic effectiveness of carbamazepine is generally very rapid in the treatment of seizure and paroxysmal pain disorders, shows some lag in the treatment of mania, and exhibits the longest lag in depression. These time course variations may indicate that different mechanisms underlie the efficacy of carbamazepine in the differential neuropsychiatric syndromes. Biochemical and pharmacological data suggest that the anticonvulsant effects of carbamazepine are related to "peripheral-type" benzodiazepine and alpha 2-noradrenergic receptor systems and to its ability to stabilize sodium channels. GABAB (baclofen-like) actions appear to be involved in antinociceptive, but not anticonvulsant, effects. The relatively acute time course of antimanic efficacy may be related to the above-mentioned mechanisms or to other effects related to systems postulated to be altered in the manic syndrome. These effects might include carbamazepine's ability to increase acetylcholine in the striatum, decrease probenecid-induced levels of CSF homovanillic acid (HVA) in man and dopamine turnover in animals, decrease CSF norepinephrine in manic patients, inhibit adenylate cyclase activity (in response to norepinephrine, dopamine, adenosine, or ouabain), decrease GABA turnover, or act as a vasopressin agonist. Efficacy in depression may be related to actions in man that take time or chronic drug administration to develop, such as increases in plasma tryptophan, decreases in CSF somatostatin, decreases in thyroid indices, and increases in urinary free cortisol excretion and, in animals, increases in substance P sensitivity and increases in brain adenosine receptors. The ability of carbamazepine to block the development of lidocaine- and cocaine-induced seizures also requires chronic administration, suggesting that these seizure models may provide a unique perspective for understanding mechanisms of time-dependent effects.
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PMID:Time course of clinical effects of carbamazepine: implications for mechanisms of action. 328 May 60

The effects of peptides on brain function suggest therapeutic and pathologic roles for these substances. Many peptides cross the blood-brain barrier (BBB) by transmembrane diffusion as a function of their lipid solubilities. Other peptides, such as the enkephalins, Tyr-MIF-1, vasopressin-related peptides, and peptide T-like peptides, are transported by carrier-mediated systems. Passage is influenced by aging, stress, lighting, drugs, amino acids, and neurotoxins. Disruption of the BBB results in complex changes in the blood and CSF levels of peptides. Peptides influence the passage of glucose, amino acids, and inorganic acids and may affect the integrity of the BBB. Peptide-BBB interactions have been suggested to play direct roles in dialysis dementia and maple syrup urine disease; they may be expected to be involved in other disorders of the CNS.
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PMID:Interactions between the blood-brain barrier and endogenous peptides: emerging clinical implications. 328 19

Lysine-vasopressin (LVP) at different concentrations (2 ng, 200 pg) was injected into the lateral ventricle and cisterna magna. The effect on hypothalamic self-stimulation was studied in rats. LVP (2 ng) decreased the self-stimulation rate after intracerebroventricular and cisternal application. Injection of 200 pg LVP diminished the self-stimulation rate after cisternal administration only. The findings suggest that the site of peptide administration is of decisive importance to vasopressin-induced effects. Both biochemical factors and the interaction between behaviour and vegetative nervous system should be taken into consideration when interpreting changes in self-stimulation as induced by vasopressin applied to the CSF space.
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PMID:Influence of intracerebroventricularly and intracisternally administered vasopressin on the hypothalamic self-stimulation rate of the rat. 343 70


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