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 suprachiasmatic nucleus (SCN) and the intergeniculate leaflet (IGL) are retinorecipient structures that play important roles in the expression of circadian rhythmicity. We examined these two structures in a diurnal ground squirrel, Spermophilus lateralis, using immunohistochemical techniques, and cholera toxin-bound horseradish peroxidase. A number of immunoreactive substances are distributed within the ground squirrel SCN in a pattern similar to that reported in many other mammals. These include vasopressin, vasoactive intestinal polypeptide, serotonin, neuropeptide Y (NPY), and glial fibrillary acidic protein. The squirrel SCN differs from that of most other species examined to date in two respects. First, a dense cluster of cells containing immunoreactive L-enkephalin (L-ENK-IR) is observed in the center of the SCN. Second, there is a contralateral, but no ipsilateral, projection from the retina to the SCN. In the lateral geniculate region there is a substantial region that contains NPY-immunoreactive cells and receives a bilateral retinal projection. This region is assumed to be homologous with the IGL described in other mammals. Cells containing L-ENK-IR are distributed throughout the LGN in groups that overlap, but which have a distinctly different distribution than the more extensive groups of NPY-IR cells.
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PMID:Immunocytochemical characterization of the suprachiasmatic nucleus and the intergeniculate leaflet in the diurnal ground squirrel, Spermophilus lateralis. 172 27

Surgical isolation of the suprachiasmatic nuclei (SCN) within a hypothalamic island is reported to produce loss of circadian rhythmicity. The results have been interpreted to indicate that SCN efferents are necessary for the expression of circadian rhythms. It is not clear, however, whether the loss of circadian rhythms in behavioral responses following SCN isolation is attributable to transection of efferents, to loss of cells within the island, or to gliosis produced by the knife cut. To explore this issue, we examined locomotor activity and gonadal state of male golden hamsters housed in constant darkness (DD, with a dim red light for maintenance) for at least 10 weeks following isolation of the SCN from the rest of the brain by cuts by means of a Halasz wire microknife. Brain sections were immunocytochemically stained for the peptides vasoactive intestinal polypeptide (VIP), vasopressin (VP) or neurophysin II (NP II), and neuropeptide Y (NPY) to localize the SCN and to assess its viability, and for glial fibrillary acidic protein (GFAP) to delimit the border of the knife cut. Experimental animals with VIP and VP/NP II immunoreactivity in the SCN within the island retained free-running locomotor rhythms following transection of SCN efferents. Animals with cuts that failed to sever SCN efferents, and sham-operated animals (in which the Halasz knife was lowered but not rotated), also maintained circadian rhythmicity. Hamsters sustaining severe damage to the SCN showed disrupted locomotor activity. In those hamsters that retained circadian locomotor rhythmicity following SCN isolation, gonads failed to regress in DD, demonstrating the absence of an appropriate photoperiodic response. The results suggest a multiplicity of SCN coupling mechanisms in the control of circadian rhythms.
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PMID:Circadian locomotor rhythms, but not photoperiodic responses, survive surgical isolation of the SCN in hamsters. 177 90

When men are exposed to a hyperbaric environment, urine flow increases. In order to elucidate the mechanism of this hyperbaric diuresis, a dry saturation dive experiment was carried out. Five male subjects were exposed to a 16-21 ATA (atmospheric pressure absolute) helium-oxygen (He-O2) environment for 4 days. Five blood samples were obtained in the early morning (0600-0630 h): once at predive 1 ATA air, 3 times at 16-21 ATA He-O2, and once at postdive 1 ATA air. Eight-hour timed urine samples, 0600-1400 h, 1400-2200 h, and 2200-0600 h (night urine), were collected throughout the experimental period. Urine flow markedly increased by the exposure to hyperbaria in the presence of constant creatinine clearance. The increase was mostly attributable to the urine flow during 2200-0600 h. The secretion of antidiuretic hormone (ADH) was suppressed at daytime and night during the exposure. On the other hand, the secretion of atrial natriuretic polypeptide (ANP) increased solely at night during hyperbaria and correlated with the increases of both the nocturnal urine flow and the nocturnal urinary excretion of sodium. These results suggest that both suppressed ADH secretion and stimulated ANP secretion cause hyperbaric diuresis.
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PMID:Hyperbaric diuresis is associated with decreased antidiuretic hormone and increased atrial natriuretic polypeptide in humans. 183 Mar 48

The mechanism of polyuria associated with paroxysmal supraventricular tachycardia (SVT) was investigated in 8 patients. SVT was induced artificially and sustained for 60 minutes. Urine and blood samples were collected every 30 minutes. During the latter half of SVT, urine flow increased twofold in the control subjects before SVT. Urinary sodium excretion increased significantly (p less than 0.01) within 30 minutes after SVT. Urinary excretion of antidiuretic hormone (ADH) decreased (p less than 0.01) during the latter half of SVT and increased (p less than 0.01) after SVT, respectively. Plasma level of ADH did not change during SVT but increased (p less than 0.05) after SVT. The concentration of plasma atrial natriuretic polypeptide (ANP) increased significantly (p less than 0.05) before SVT ended. Urinary excretion of prostaglandin E2 increased significantly (p less than 0.05) after termination of SVT. The percent changes in the urinary excretion of prostaglandin E2 were correlated (r = 0.713, p less than 0.001) with those of ADH. There was also a correlation (r = 0.6, p less than 0.001) between the percent changes in the urinary excretion of prostaglandin E2 and those of sodium. Their findings suggest that the polyuria during SVT is attributed mainly to the inhibition of ADH release and that the natriuresis after SVT is due not only to the increased ANP but also to the increased renal prostaglandin E2 probably stimulated by ADH.
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PMID:Different mechanisms of polyuria and natriuresis associated with paroxysmal supraventricular tachycardia. 183 Apr 49

Although synthetic atrial natriuretic polypeptide (ANP) is known to influence the water and electrolyte metabolism and arginine-8-vasopressin (AVP) secretion, the physiological role of endogenous ANP in the rat brain is still unclear. Accordingly, an investigation was made of the effects of intracerebroventricular (icv) administration of human h-ANP antiserum, which can neutralize endogenous ANP, on the water intake, urine output, urinary excretion of potassium and sodium, and plasma AVP level in normally hydrated rats. Apart from the water intake, all the parameters were also determined in 48-h water-deprived rats after h-ANP antiserum treatment. The icv administration of the h-ANP antiserum significantly increased the spontaneous water intake, urine output and urinary potassium excretion in rats given water ad libitum. These effects developed by 24 h after icv treatment. The h-ANP antiserum had no effect on the urine volume in 48-h water-deprived rats, suggesting a primary effect of endogenous ANP in the brain on the spontaneous water intake in rats given water ad libitum. These results suggest that ANP may have a physiologically important role in the central regulation of the water and electrolyte metabolism. The h-ANP antiserum did not alter the basal and dehydration-induced AVP release. This raises the possibility that the endogenous ANP in the brain may not participate in the control of AVP secretion.
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PMID:Central effects of antiserum against human atrial natriuretic polypeptide on water and electrolyte metabolism and plasma arginine-8-vasopressin level in conscious rats. 183 49

It was investigated whether the secretion of epinephrine, norepinephrine, and arginine vasopressin from the adrenal medulla, sympathetic nerve endings, and posterior pituitary gland, respectively, was involved in the mediation of the pressor effect of intracerebroventricular (icv) administration of vasoactive intestinal polypeptide (VIP) in anesthetized rats. Icv administration of 1 microgram VIP increased mean blood pressure by 21% and heart rate by 17% in Wistar rats although the lesser dose was effective only for increasing heart rate. Simultaneously with the change in blood pressure and heart rate, the concentrations of plasma epinephrine and norepinephrine rose 4 and 10 min after VIP administration. After adrenalectomy, the action of VIP on mean blood pressure or heart rate was unchanged or partially reduced, respectively. Although the cardiovascular action of VIP was observed in control Long-Evans rats as well as in Brattleboro rats homozygous or heterozygous for diabetes insipidus, which hereditarily lacked vasopressin completely or partially, the increase in mean blood pressure after icv administration of VIP was more marked in homozygous than heterozygous rats or Long-Evans rats. These results suggest that the cardiovascular action of centrally administered VIP is mediated by increased sympathetic nerve outflows including stimulation of adrenal epinephrine secretion and is enhanced by the chronic absence of vasopressin secretion from the posterior pituitary gland.
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PMID:Mechanism for the cardiovascular action of intracerebroventricularly administered vasoactive intestinal polypeptide in rats. 186 14

The anterograde Phaseolus vulgaris-leucoagglutinin (PHA-L) tracing technique was used to determine the distribution of efferent fibers originating in the lateral septal nucleus of the guinea pig. For complementary detection of the chemical identity of the target neurons, double-labeling immunocytochemistry was performed with antibodies to PHA-L and to vasopressin, oxytocin, vasoactive intestinal polypeptide, serotonin or dopamine beta-hydroxylase, respectively. The hypothalamus received the majority of the PHA-L-stained septofugal fibers. Here, a specific topography was observed. (1) The medial and lateral preoptic area, (2) the anterior, lateral, dorsal, posterior hypothalamic and retrochiasmatic area, (3) the supraoptic, paraventricular, suprachiasmatic, dorsomedial, caudal ventromedial and arcuate nuclei, and (4) the tuberomammillary, medial and lateral supramammillary, dorsal and ventral premammillary nuclei always contained PHA-L-labeled fibers. The rostral portion of the ventromedial nucleus and the medial and lateral mammillary nucleus only occasionally showed weak terminal labeling. In other diencephalic areas, termination of PHA-L-labeled fibers was observed in the epithalamus and the nuclei of the midline region of the thalamus. In the mesencephalon, terminal varicosities occurred in the ventral tegmental area, interfascicular and interpeduncular nucleus, and periaqueductal gray. In addition, the dorsal and medial raphe nuclei of the metencephalon, together with the locus coeruleus and the dorsal tegmental nucleus, received lateral septal efferents.
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PMID:The efferent connections of the lateral septal nucleus in the guinea pig: projections to the diencephalon and brainstem. 186 17

This review summarizes the revolutionary impact of brain peptides on our understanding of the nervous system and then discusses the localization, distribution, synthesis, receptor sites, and possible function of 32 brain peptides. The peptides are discussed in three subgroups: I) the opioid peptides, which include beta-endorphin, the enkephalins, and dynorphin; II) the pituitary releasing hormones, most of which are wide-spread in the brain and include corticotropin-releasing hormone, luteinizing hormone-releasing hormone, somatostatin, and thyrotropin-releasing hormone; and III) a selection of 12 other peptides potentially important for neurological function, including vasopressin, oxytocin, substance P, cholecystokinin, bombesin, neurotensin, renin, angiotensin, vasoactive intestinal polypeptide, neuropeptide Y, calcitonin gene-related peptide, and calcitonin. Within each individual peptide section, the possible physiological roles in anterior pituitary hormone release, blood-flow regulation, feeding behavior, temperature regulation, nociception, memory and learning, and movement are reviewed. Further, where noted, the peptide findings in Huntington's, Alzheimer's, Parkinson's and psychiatric diseases are emphasized.
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PMID:Neuropeptides. 187 Jul 24

This paper summarizes the recent knowledge on the factors stimulating or inhibiting the adrenocortical growth. In the part I of the present review the following stimulatory growth factors are discussed: ACTH--in vivo, N-POMC derivatives, dibutyryl cAMP--in vivo, GH, Prl, vasopressin, oxytocin, insulin, insulin-like growth factor I (somatomedin C), estradiol and vasoactive intestinal polypeptide (VIP). Among the factors, which inhibit the adrenocortical growth, the following ones are considered: ACTH--in vitro, cAMP--in vitro, adrenal steroids and testicular androgens. The remaining hormones and factors affecting the adrenocortical growth are described in the part II of the review.
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PMID:[Factors stimulating and/or inhibiting growth processes of the adrenal cortex. I. The role of the anterior pituitary and hypothalamic hormones, insulin, sex steroids and certain neuropeptides]. 194 99

The modulation of Ca2+ currents by neurotransmitters was studied in freshly dissociated rat spinal cord neurons, using the whole-cell patch-clamp technique. GABA, baclofen, adenosine, ATP, serotonin, norepinephrine, somatostatin, and dynorphin A inhibited the current through Ca2+ channels in a substantial fraction of cells, while substance P, vasoactive intestinal polypeptide, [D-ala2,d-leu5]-enkephalin, cholecystokinin-8 (sulfated), calcitonin gene-related peptide, angiotensin II, neurotensin, vasopressin, and thyrotropin-releasing hormone had no effect. In the case of baclofen, the inhibition is mediated, at least in part, by a GTP-binding protein. Suppression of Ca2+ current by neurotransmitters may represent a mechanism of presynaptic inhibition in the spinal cord.
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PMID:Neurotransmitter modulation of calcium current in rat spinal cord neurons. 196 36


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