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 present study continues a previous investigation on the median eminence (EM) (Krisch et al., 1978). In rats with high levels of neurohormones (LHRH, vasopressin) a limited immunohistochemical labeling of perivascular tanycyte processes can be observed surrounding capillaries in the marginal region of the organum vasculosum laminae terminalis (OVLT) and in the inner part of the subfornical organ (SFO). This labeling extends from the perivascular space a short distance along the tanycyte processes. By conventional electron microscopy and by freeze-etching, tight junctions are demonstrated at a distance from the capillary lumen which corresponds to the borderline of the immunohistochemical labeling of perivascular tanycyte processes in light microscopic preparations. The tight junctions are arranged in several parallel and helical rows and correspond to those found in the median eminence. Consequently, the immunohistochemical labeling the OVLT and in the SFO marks the intercellular cleft. In the circumventricular organs the immunostaining labels the extension of the perivascular space characterized by the hemal milieu. The perivascular space is separated off by tight junctions from the CSF-milieu of the adjacent neuropil. Furthermore, the present study demonstrates tight junctions in the marginal region of the area postrema (AP) between the perivascular processes of the tanycytes.
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PMID:The functional and structural border between the CSF- and blood-milieu in the circumventricular organs (organum vasculosum laminae terminalis, subfornical organ, area postrema) of the rat. 36 50

In 1975, during the largest epidemic of St Louis encephalitis (SLE) in the United States, 416 cases were diagnosed in Ohio. Persons who were admitted to two Columbus (Ohio) hospitals with suspected acute viral CNS infection were prospectively studied to define the virologic and clinical aspects of SLE. Sixteen cases of SLE were diagnosed serologically. Fifteen patients had signs of encephalitis and one had aseptic meningitis. Six patients had the syndrome of inappropriate antidiuretic hormone secretion. Other frequent findings included moderate peripheral leukocytosis and CSF pleocytosis, with mild elevation of CSF protein levels but normal glucose levels. Severe neurologic sequelae were infrequent. The EEG proved valuable in diagnosis and prognosis. Results of brain scans were normal. Virus in CSF or urine was not demonstrated, nor was viral antigen in CSF or urine sediments. Specific antibody was found in the sera and CSF of all patients who were tested, but interferon was not detected.
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PMID:St Louis encephalitis in Ohio, September 1975: clinical and EEG studies in 16 cases. 44 51

In non-hydrated goats prolonged (3 h, 0.02 ml/min) intracerebroventricular (IVT) infusion of 0.35 M glycerol depressed the plasma vasopressin level during the entire infusion period which resulted in a conspicuous water diuresis outlasting the infusion by about 20 min. Since no compensatory drinking occurred during this sustained water diuresis it gradually induced pronounced dehydration (loss of greater than 1 liter of total body water causing 5% increase in plasma [Na+] and osmolality). The same degree of dehydration was in other experiments induced by water deprivation. It then caused a 5-fold increase in plasma vasopressin level. Corresponding IVT infusions of 0.35 M d-glucose depressed plasma vasopressin level only during the first half of the 3 h infusion period. Consequently, the resulting water diuresis was transient and subsided before the glucose infusion was finished. Plasma renin activity increased during the IVT glycerol infusion and during water deprivation, but was largely unaffected by IVT glucose. Both IVT glycerol and glucose decreased renal sodium excretion. The possibility is discussed that the pronounced ability of IVT glycerol to depress the vasopressin release and thirst is not only due to dilution induced reduction of CSF [Na+], but also to an influence of glycerol on choroidal and/or transependymal Na+-transporting mechanisms.
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PMID:Inhibition of vasopressin-release during developing hypernatremia and plasma hyperosmolality: an effect of intracerebroventricular glycerol. 65 32

Angiotensin II injected in small doses into the cerebral ventricles produces an increase in blood pressure and drinking behavior. The site of action for both of these effects was studied in 3 main experiments. (1) The response to several doses of angiotensin delivered to each ventricle was investigated with multiple ventricular cannulation. This revealed that the rostral ventricular system was involved in angiotensin II mediated responses. (2) CSF flow was limited by plugging specific anterior and posterior ventricular regions and then testing for angiotensin II induced drinking and pressor responses. This technique showed that the ventral anterior third ventricle must be reached by the peptide in order to produce either blood pressure or drinking effects. (3) In order to separate pressor components due to vasopressin release and sympathetic activation, hypophysectomized rats were also tested. The experiment showed that the pressor response to intraventricular angiotensin II is due to both sympathetic and pituitary hormonal components and both are dependent on sites sensitive to angiotensin in the anterior third ventricule. The ventral anterior third ventricle or periventricular tissue surrounding it seems to be essential for both blood pressure and drinking responses to intraventricular angiotensin II.
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PMID:Regional study of cerebral ventricle sensitive sites to angiotensin II. 93 46

Infusions of isotonic or hypertonic (0.3 or 0.5 M) glycerol into the lateral cerebral ventricle (60 min, 0.02 ml/min) of non-hydrated goats invariably induced a conspicuous and sustained water diuresis. Corresponding infusions of 0.3 M glycerol/0.16 M NaCl were almost equally efficient in this respect. A more short-lasting and less pronounced water diuresis was obtained in response to equivalent infusions of pure d-glucose, and the response to 0.3 M glucose/0.16 M NaCl was variable. Intravenous injections of vasopressin blocked the glucose-induced diuresis, but only postponed the glycerol-induced diuresis. Intracerebroventricular (IVT) infusions of 0.5 M glycerol caused a sustained, complete inhibition of the urge to drink in the 48 h dehydrated goat, whereas IVT glucose only attenuated dehydrative drinking. Twenty min after the infusions of glycerol the CSF [Na+] in the lateral ventricle was about 15% below normal. About 10% reduction of CSF [Na+] was obtained 20 min after the IVT infusion of glycerol/NaCl. The corresponding infusion of pure d-glucose reduced the CSF [Na+] by less than 5%. The glycerol and glycerol/NaCl infusions caused a moderate reduction of renal Na+ + K+ excretion. The possibility is discussed that the observed effects of IVT glycerol is a manifestation of its efficiency to inhibit choroidal and/or juxtaventricular (Na+-K+)-ATPase activity.
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PMID:Intracerebroventricular glycerol: a potent inhibitor of ADH-release and thirst. 99 97

To clarify the cardiovascular effects of central vasopressin (AVP), a chronic intracerebroventricular (ICV) infusion of AVP was performed in conscious Wistar normotensive rats. Animals were divided into 3 groups: 1) AVP 1 ng/hr (Low), 2) AVP 100 ng/hr (High), and 3) saline (control) ICV infusion. After a 6 day control period, AVP or saline was continuously infused into the lateral cerebroventricle at a rate of 1 microliter/hr using osmotic minipump for 7 days. As a result, a dose-related elevation of AVP concentration in CSF was achieved. Systolic blood pressure in both Low and High AVP infusion was slightly (7-12 mmHg) but significantly higher than that in control. ICV infusion of AVP did not alter urine volume, electrolytes excretion or osmolality, and AVP vascular antagonist injected intravenously failed to affect mean arterial pressure. Furthermore, plasma catecholamines and renin activity did not differ significantly among the groups. Thus, chronic ICV infusion of AVP induced the elevation of blood pressure, which is due to centrally mediated effect of AVP.
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PMID:Chronic cardiovascular effects of central vasopressin in conscious rats. 135 44

Corticotropin-releasing hormone (CRH), somatostatin (SOM), delta-sleep-inducing peptide (DSIP), neuropeptide Y (NPY), beta-endorphin (beta-END), and vasopressin (AVP), which are regarded as being involved in the HPA-regulation were investigated in lumbar CSF of 44 suicide attempters. The patients were diagnosed according to the DSM-III-R, and rated with the MADRS. The neuropeptides were compared with the serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA) in CSF and with post-dexamethasone plasma cortisol. We found strong correlations between CRH and the peptides SOM and beta-END. The latter also correlated positively with SOM. There were no differences between men and women. Patients with major depressive disorders had significantly lower SOM, CRH, and DSIP than other patients. Both SOM and beta-END correlated negatively with post dexamethasone plasma cortisol in all patients. We found no significant relationships between neuropeptides and CSF 5-HIAA. Patients who had made previous suicide attempts had significantly lower CRH than those who had not. No other significant associations between neuropeptides and suicidal subgroups of patients appeared, and there was no indication of specific neuropeptide patterns in patients who later completed suicide. Intercorrelations of some neuropeptides and low SOM and DSIP in major depressed patients are findings in line with those by others.
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PMID:HPA-related CSF neuropeptides in suicide attempters. 137 70

The CSF is often regarded as merely a mechanical support for the brain, as well as an unspecific sink for waste products from the CNS. New methodology in receptor autoradiography, immunohistochemistry and molecular biology has revealed the presence of many different neuroendocrine substances or their corresponding receptors in the main CSF-forming structure, the choroid plexus. Both older research on the sympathetic nerves and recent studies of peptide neurotransmitters in the choroid plexus support a neurogenic regulation of choroid plexus CSF production and other transport functions. Among the endocrine substances present in blood and CSF, 5-HT, ANP, vasopressin and the IGFs have high receptor concentrations in the choroid plexus and have been shown to influence choroid plexus function. Finally, the choroid plexus produces the growth factor IGF-II and a number of transport proteins, most importantly transthyretin, that might regulate hormone transport from blood to brain. These studies suggest that the choroid plexus-CSF system could constitute an important pathway for neuroendocrine signalling in the brain, although clearcut evidence for such a role is still largely lacking.
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PMID:Neuroendocrine regulatory mechanisms in the choroid plexus-cerebrospinal fluid system. 139 90

The effect of central administration of AII on CSF formation was studied in alpha-chloralose and urethane anesthetized rabbits using the ventriculocisternal perfusion method. AII infused i.c.v. at rates of 5.5 and 55 pg/min significantly decreased CSF production by 25% and 35%, respectively. In contrast, AII when given at 5.5 ng/min did not change CSF formation. It seems that drop in CSF production observed during central administration of AII at low doses is mediated by both increased vasopressin release and activation of the sympathetic nervous system. The lack of changes in CSF formation with the highest AII dose used is not clear at present and awaits further investigation. Specific AII antagonist, saralasin, was found to significantly increase CSF production in four of five animals studied. It is suggested that in normal conditions AII may exert a tonic inhibitory effect on CSF formation.
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PMID:Effect of central administration of angiotensin II on cerebrospinal fluid formation in rabbits. 141 Apr 4

It is clear that the behavioral actions of oxytocin and vasopressin in mammals are not newly acquired, but have evolutionary antecedents. Injection studies with fish, amphibians, reptiles, and birds indicate that AVT can activate certain reproductive behaviors. The strongest evidence that AVT acts centrally to control reproductive behaviors comes from research on T. granulosa. In this amphibian, injections of AVT agonists activate courtship behaviors (amplectic clasping) in males and egg-laying behaviors in females, whereas injections of AVT antagonists inhibit the behaviors. Also, in Taricha males, AVT concentrations in specific brain areas are associated with the expression of courtship behaviors. Several conclusions about steroid-peptide interactions can be drawn, based on research with this amphibian. First, gonadal steroid hormones act to maintain the behavioral actions of AVT in both males and females. In Taricha, gonadectomy abolishes and steroid implants restore AVT-induced courtship in males and egg-laying in females. Second, gonadal steroids maintain the behavioral actions of AVT, in part, by modulating AVT receptor numbers on target neurons. In Taricha males and females, gonadectomy reduces AVT receptor concentrations (but not binding affinity) in certain brain areas (amygdala pars lateralis) and not others. Third, the type of gonadal steroid determines whether AVT elicits male-like or female-like reproductive behaviors. Ovariectomized Taricha females respond to AVT injections with egg-laying behaviors when implanted with estradiol and with male-like amplectic clasping when implanted with dihydrotestosterone. Fourth, the masculinization of AVT-induced behaviors in females most likely reflects site-specific actions of androgens on AVT-synthesizing neurons. In Taricha, AVTir concentrations in the optic tectum are sexually dimorphic (higher in males than females) and reach peak levels in males during the breeding season. Fifth, AVT content in specific brain areas increase as a function of performing the behaviors. In Taricha, AVTir concentrations in DPOA, CSF, and ventral infundibulum are higher in males that exhibit courtship behaviors than in males that do not. These conclusions illustrate how steroid-peptide interactions in the control of behaviors entail multiple neuroanatomical sites and neurochemical actions.
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PMID:Evolutionary precedents for behavioral actions of oxytocin and vasopressin. 162 27


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