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Medline ® Abstracts for References 1,6,7

of 'Vasopressin and desmopressin stimulation test'

1
TI
Vasopressinergic and oxytocinergic pathways in the central nervous system.
AU
Zimmerman EA, Nilaver G, Hou-Yu A, Silverman AJ
SO
Fed Proc. 1984;43(1):91.
 
Recent data obtained by immunohistochemical and other anatomical tracing methods indicate that oxytocin and vasopressin pathways are much more complex and extensive than previously recognized. In addition to the classic magnocellular neurons that project from the supraoptic and paraventricular (PVN) nuclei to the posterior pituitary gland, generally smaller neurons in various parts of the PVN send vasopressin fibers to the portal capillary bed in the median eminence, or send oxytocin or vasopressin projections to other brain and spinal cord sites. In addition, vasopressin neurons are also found in the suprachiasmatic nucleus and may contribute to extrahypothalamic projection areas. Many of these axonal projections appear to form synapses with other neurons in forebrain, hindbrain, and spinal cord regions, which suggests roles for these peptides in neuronal communication. In brain stem and spinal cord, terminal fields include both parasympathetic and sympathetic regulatory centers. Oxytocin terminals are also found on large intracerebral arteries where the peptide may regulate cerebral blood flow.
AD
PMID
6
TI
Glucocorticoid inhibition of neurohypophysial vasopressin secretion.
AU
Raff H
SO
Am J Physiol. 1987;252(4 Pt 2):R635.
 
Several lines of evidence have suggested that neurohypophysial vasopressin secretion is under the influence of glucocorticoid negative feedback. Studies in clinical and experimental adrenal insufficiency have suggested that the impaired water excretion accompanying that syndrome may be due to elevated vasopressin levels. Furthermore, both the impaired water excretion and elevated vasopressin levels observed in adrenal insufficiency may be normalized by glucocorticoid treatment. This topic remains controversial, with a considerable body of evidence suggesting that vasopressin is elevated during adrenal insufficiency not because of a loss of central steroid negative feedback but because of alterations in plasma volume osmolality (renal mechanisms). Vasopressin responses to a variety of stimuli (hemorrhage, hypoxia, hypertonic saline) in normal humans and animals appear to be attenuated or eliminated by pretreatment with glucocorticoids. However, the vasopressinergic system appears to be considerably less sensitive to negative feedback than the corticotropin-releasing factor-adrenocorticotropic hormone (ACTH) system. There is evidence that the locus for this inhibitory effect is both directly at the posterior pituitary and within the hypothalamus. It is unlikely that corticosteroid negative feedback closes a direct hypothalamo-neurohypophysial-adrenocortical feedback loop. Since neurohypophysial vasopressin is involved in the control of ACTH secretion, it is more likely that the modulation of neurohypophysial vasopressin by glucocorticoid is an integral part of the overall negative-feedback control of ACTH secretion. The physiological role of glucocorticoid inhibition of vasopressin secretion remains speculative.
AD
PMID
7
TI
Anatomical basis of thirst and vasopressin secretion.
AU
Zimmerman EA, Ma LY, Nilaver G
SO
Kidney Int Suppl. 1987;21:S14.
 
AD
PMID