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)

Neurophysin, vasopressin and oxytocin were localized in different portions of the supraopticohypophysial tract (SHT) using the unlabeled antibody enzyme technique at the ultrastructural level. In vasopressin-positive supraoptic perikarya, vasopressin and neurophysin were present in all neurosecretory granules. Within the zona interna of the median eminence, vasopressin and neurophysin were present in two populations of axons, one with granules of 1300-1500 A and one with granules of 900-1300 A. Following exposure of thin sections of median eminence to antiserum to neurophysin, reaction products were present in granules and in the extragranular cytoplasm in the axons with larger granules; in all other cases reaction product was confined to the granules. Vasopressin-positive fibers were also presented in large numbers of the zona externa of the median eminence and many terminated on the pituitary primary portal plexus. A few oxytocin fibers were present on the portal capillaries in the infundibular stalk. In the posterior pituitary all axon profiles were neurophysin positive. Neurophysin was present as both a granular and cytoplasmic pool. Vasopressin-containing axons account for 90% of the neuronal elements in the posterior pituitary and oxytocin for the remaining 10%. Findings on the subcellular distribution of these peptides are related to current theories on transport and release of neurohormones.
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PMID:Ultrastructural studies on the localization of neurohypophysial hormones and their carrier proteins. 6 Apr 34

Slices from ox neurohypophyses were incubated in a calcium-free medium with the ionophores A23187 or X537A. X537A (5 X 10(-5) mol/l) caused a marked release of vasopressin, neurophysin and protein to the medium. A23187 (2 X 10(-5) mol/l) did not cause any release by itself, but when Ca2+ was added to the medium in the presence of the ionophore, an increase in the release of vasopressin, neuorphysin and protein occurred. Release of lactate dehydrogenase and peptidase were not affected by the ionophores. The secretion caused by A23187 was abolished by D600 (a verapamil analogue) (2 X 10(-5) mol/l) whereas the effect of X537A was unchanged. The effects of X537A were strongly inhibited by removal of sodium from the medium. Re-addition of sodium to the medium caused a marked release. Gramicidin (10(-6) or 5 X 10(-5) mol/l) had no effect on secretion. Efflux of 45Ca2+ from pre-loaded slices was drastically reduced in a sodium-free medium. X537A caused an increase in the efflux rate of 45Ca2+ both in medium with a normal concentration of sodium and when slices had been incubated in a sodium-free medium. A23187 and X537A both released 45Ca2+ from a neurohypophyseal mitochondrial fraction. When sodium in a concentration of 20 mmol/l was added to this fraction, the Ca2+ accumulation was inhibited. This effect was reduced by inorganic phosphate up to a concentration of 2 mmol/l.
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PMID:Calcium and stimulus secretion coupling in the neurohypophysis. V. The effects of the Ca2+ ionophores A23187 and X537 A on vasopressin release and 45Ca2+ efflux; interactions with sodium and a verapamil analogue (D600). 6 Aug 66

Administration of pituitrin, vasopressin, and oxytocin to rats during spontaneous micturition increases diuresis and sodium excretion by reducing tubular reabsorption. In adrenalectomized rats these preparations have no diuretic effect and increased sodium excretion is observed only after administration of vasopressin. After hypophysectomy the diuretic effect of the preparations disappears but they still increase sodium excretion. It is postulated that the diuretic effect of the neurohypophyseal hormones is connected with activation of the pituitary-adrenal system, whereas some additional mechanism is involved in their effect on sodium excretion.
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PMID:Mechanism of action of neurohypophyseal hormones on sodium excretion and diuresis. 6 76

Because vascular casts of the pituitary demonstrated that there are a few venous connections from the adenohypophysis to the juxtaposed cavernous sinus, it was predicted that some portal vessels must carry blood from the adenohypophysis back to the neurohypophysis. Physiological studies confirmed this prediction and verified earlier observations that blood-flow within the neurohypophysis can be towards the median eminence. In the present study, increased concentrations of prolactin and growth hormone were found in blood sampled from intracranial vessels (internal carotid artery and sagittal sinus). It was concluded that the neurohypophyseal capillary bed not only receives trophic hormones produced in the adenohypophysis but, under certain physiological circumstances, delivers those hormones directly to the brain.
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PMID:Pituitary secretes to brain. Experiments in sheep. 6 83

Insulin-induced hypoglycaemia caused a threefold rise in plasma-arginine-vasopressin concentration (to 4-36 +/- 0-77 pmol/1) in ten subjects who had normal posterior-pituitary function. Plasma-arginine vasopressin reached a peak 30 min after injection of insulin. Plasma concentrations of arginine vasopressin obtained with hypoglycaemia were similar to those achieved after overnight dehydration for 14-16 h. No rise in plasma-arginine-vasopressin was observed in three patients with cranial diabetes insipidus in whom severe hypoglycaemia developed after insulin infusion. It is suggested that the measurement of arginine vasopressin during insulin-induced hypoglycaemia may be a useful clinical test of posterior-pituitary function.
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PMID:Plasma-arginine-vasopressin response to insulin-induced hypoglycaemia. 7 Jun 44

The concept of the "inappropriate" has a well-defined and easily comprehended meaning when applied to tumour secretion of antidiuretic hormone (A.D.H., vasopressin). When applied to high A.D.H. in other situations such as nephrotic syndrome, congestive cardiac failure, or cirrhosis, the use of the term "inappropriate secretion" simply reflects the fact that an easily measured controlling factor (plasma tonicity) is being overridden by a less easily measured one (effective extracellular volume). Similarly, sodium excretion in hypertension is said to be inappropriately low for the raised renal perfusion pressure: in this case inappropriateness results from the antinatriuretic effect of a minor degree of sodium depletion produced by pressure natriuresis. A similar objection can be made to the application of the term to the relations between renin or angiotensin-II concentrations and blood-pressure in some forms of hypertension. Since inappropriateness merely reflects the position and predilections of the observer, the widespread use of the term should be abandoned.
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PMID:On the inappropriate in hypertension research. 7 8

Plasma concentrations of arginine-vasopressin (antidiuretic hormone) have been measured in 40 patients with benign essential hypertension and 12 patients with malignant-phase hypertension. Values tended to be low in the benign phase and high in the malignant phase. 5 normal subjects were infused with synthetic arginine-vasopressin, producing plasma concentrations up to five times the highest value recorded in malignant-phase hypertension, without any effect on blood-pressure. There is no evidence that vasopressin has a direct role in the pathogenesis of benign essential hypertension or its transition to the malignant phase. On the contrary, abnormal vasopressin concentrations may be caused by hypertension.
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PMID:Changes of vasopressin in hypertension: Cause or effect? 7 91

The spleen of each of 20 mongrel dogs was traumatized by creating a wedge laceration, and selective arterial infusion was then performed with vasopressin in four dogs, pituitrin in eight, and epinephrine in eight. Infusion therapy with vasoconstrictors controlled the splenic hemorrhage in 19 of 20 dogs. The 15 dogs surviving the experimental period of four to eight weeks showed well-healed scars at the sites of lacerations. Three dogs had small contracted spleens as a result of massive infarction. The results of this experiment indicate that splenic hemorrhage in the experimental dogs can be controlled by selective infusion of pituitrin or vasopressin, but is more effectively controlled with epinephrine.
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PMID:Selective arterial infusion of vasoconstrictors for control of traumatic splenic hemorrhage. 7 66

17 patients with severe hyponatraemia (none had cardiac failure or had lately had an operation) all had excessively high plasma-antidiuretic hormone (A.D.H.). Only 13 had features typical of the syndrome of inappropriate secretion of A.D.H. (S.I.A.D.H.). Plasma-A.D.H. was not related to either plasma-sodium or diagnosis. There were as many patients with chest infection as with carcinoma of the lung. Plasma-sodium and plasma-A.D.H. returned rapidly towards normal in the patients with chest infection or volume depletion but these concentrations corrected much more slowly in patients with carcinoma of the lung. The increase in plasma-sodium in patients with chest infection was too rapid to be produced by water-deprivation treatment and was due to return of plasma-A.D.H. to normal. The term S.I.A.D.H. implies an understanding of pathophysiology that does not exist. As a diagnosis it does not help in management or prognosis. A simpler, more descriptive terminology such as "hyponatraemia with carcinoma of the lung" would be more useful and less confusing in the clinical situation.
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PMID:Severe hyponatraemia. A study of 17 patients. 7 64

Animal studies have revealed two important aspects of vasopressin function which make this peptide a suitable candidate for involvement in complex behavioural syndromes: (1) vasopressin deficiency produces deficits of behaviour which are reversed by vasopressin; (2) well-developed systems exist for the distribution of vasopressin throughout the central nervous system (C.N.S.) via either peptidergic neurons or the cerebrospinal fluid (C.S.F.) and provide the means by which vasopressin may regulate cells controlling behavioural or physiological processes. Among the processes which vasopressin can influence are several of significance in the symptom-complex of affective illness, including alterations in memory, changes in pain sensitivity, synchronisation of biological rhythms, the timing and quality of R.E.M. sleep, and the regulation of fluid and electrolyte balance. In addition, vasopressin is functionally linked to monoamine neurotransmitter systems and, like them, is altered by pharmacological agents which affect mood. Some of the pharmacological and clinical data suggest that vasopressin function is diminished in depression and augmented in mania; sometimes, however, alterations in vasopressin function may be detectable only during crucial periods of the manic-depressive cycle. The hypothesis that vasopressin plays a role in disorders of human behaviour, particularly manic-depressive illness, can now be directly tested by radioimmunoassays of vasopressin in C.S.F. and plasma and by the administration of specific vasopressin analogues and inhibitors.
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PMID:Vasopressin in affective illness. 7 97


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