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)

Lesions of the brain region surrounding the anteroventral third ventricle (AV3V) have been shown to result in adipsia without a corresponding antidiuretic response or rise in plasma vasopressin levels. Electron microscopic examination of the supraoptic nucleus and neural lobe of the pituitary has shown that large stores of neurosecretory material build up in the neurohypophysis. In the present study, the increased neurosecretory material was characterized by immunocytochemistry. Vasopressin immunoreactivity was examined and compared between adipsic rats with AV3V lesions, water-deprived rats, and normal rats. Two days after surgery, sham-lesioned, water-deprived rats displayed decreased vasopressin immunostaining density compared to normal controls, and adipsic AV3V-lesioned rats displayed increased vasopressin immunoreactivity throughout the magnocellular-hypophyseal system. These results indicate that AV3V lesions interrupt neural inputs that stimulate the magnocellular system to release vasopressin in response to normal humoral stimuli.
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PMID:Changes in magnocellular-neurohypophyseal vasopressin following anteroventral third-ventricle (AV3V) lesions. 243 77

We lesioned the periventricular tissue of the anteroventral portion of the third cerebral ventricle (AV3V) of dogs to evaluate the mechanism that accounts for blunting of the pressor activity of angiotensin II (ANG II). AV3V lesions were done with a microknife using a transbuccal approach; the procedure denervated the organum vasculosum of the laminae terminalis, the nucleus medianus, and the medial preoptic nucleus. Two to four days after surgery, the conscious AV3V-lesioned dogs showed adipsia and their blood contained increased quantities of Na+ (175 +/- 2 meq/l) and an elevated osmolality (352 +/- 5 mosmol/kg). Cardiac rate was faster (131 +/- 8 beats/min) in AV3V-lesioned dogs, but their mean arterial pressure (MAP) was within normal values (99 +/- 4 mmHg). These changes were accompanied by an almost 18-fold increase in the plasma levels of immunoreactive ANG II (irANG II). In contrast, plasma vasopressin (AVP) levels fell to nondetectable values. Pressor responses produced by intravenous infusions of ANG II or injections of norepinephrine (NE) were significantly blunted 3 days after AV3V ablation. Short-term treatment of eight AV3V-lesioned dogs with the synthetic AVP analogue, 1-desamino-8-D-arginine vasopressin, reduced plasma Na+ and irANG II levels. The pressor activity of peripheral infusions of ANG II was restored to prelesion values, whereas pressor responsiveness to NE remained depressed. These data suggest that the blunting of the pressor action of ANG II in AV3V-lesioned dogs is an expression of a disorder in the regulation of renal and behavioral mechanisms maintaining fluid balance and AVP secretion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Alternative mechanism for attenuated pressor responses in AV3V-lesioned dogs. 276 63

Nine elderly patients, some with preceding dementia, presented with adipsia, progressive dehydration, impaired consciousness, and hypernatremia following common acute infections without gastrointestinal disturbance. Studies before rehydration revealed inappropriately low plasma arginine-vasopressin (AVP) levels for plasma osmolality, insufficiently concentrated urine, absolutely or relatively low plasma angiotensin II (A-II) concentrations (compared with plasma renin activity and plasma angiotensin I concentrations), and low serum angiotensin I-converting enzyme activities. The plasma AVP concentrations were positively correlated with the plasma A-II concentrations (r = .677) but not with plasma osmolality. The plasma AVP level was raised by an intravenous infusion of A-II in one patient. These findings suggest the following sequence of events: impaired A-II production caused impairment of thirst perception, renal-concentrating capacity, and AVP secretion and contributed to development of hypernatremic dehydration in these elderly patients.
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PMID:Impaired arginine-vasopressin secretion associated with hypoangiotensinemia in hypernatremic dehydrated elderly patients. 327 39

A male, aged 16, with chronic hypernatremia, adipsia, polyphagia, and poikilothermia was studied regarding regulation and secretion of arginine vasopressin. During recumbency at night, low plasma arginine vasopressin levels and increased volumes of dilute urine were found; whereas plasma arginine vasopressin levels and urine osmolalities rose and urine volumes decreased during ambulation in the daytime. Neither a 25% reduction of mean arterial pressure nor hypertonic saline infusion increased plasma arginine vasopressin or urine osmolalities. Treatment with 1-desamino-D-arginine-vasopressin at 6 p.m. and a scheduled fluid intake according to actual body weight eradicated hypernatremia and hyperosmolality. These data demonstrate a complete loss of arginine vasopressin secretion to osmotic stimulation, a partial defect of arginine vasopressin secretion to non-osmotic stimulation, an abolished response to stimulation of high-pressure-baroreceptors, but an intact responsiveness to stimulation of low-pressure-baroreceptors.
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PMID:Recumbent cranial diabetes insipidus. Studies in a patient with adipsia, hypernatremia, poikilothermia and polyphagia. 347 Oct 44

Fluid balance, systolic blood pressure (BP) and serum vasopressin (VP) and renin activity (SRA) in the basal state and in response to blood volume depletion were examined in unanesthetized rats previously given intrathecal 6-hydroxydopamine (6-OHDA) to destroy catecholaminergic (CA) input to supraoptic nucleus (SON). Sham-operated rats, unoperated ad libitum hydrated rats and rats undergoing 4 days of water deprivation served as controls. The 6-OHDA lesion resulted in adipsia, a failure to conserve administered fluids and a decrease in systolic BP. Despite decreased blood volume secondary to dehydration, and decreased systolic BP, the 6-OHDA group failed to show the expected increase in serum VP. However, when blood volume was further decreased following intraperitoneal polyethylene glycol, lesioned rats showed robust VP and SRA responses. Thus, CA input to critical target areas in the hypothalamus may be necessary for maintenance of sensitivity to stimuli that normally elicit VP release. Decreased systolic BP following 6-OHDA lesions most likely results from dehydration coupled with inadequate VP responses.
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PMID:Effects of lesions of hypothalamic catecholamines on blood pressure, fluid balance, vasopressin and renin in the rat. 355 13

Lesions of the periventricular tissue surrounding the anteroventral third ventricle (AV3V) have been shown to disrupt body fluid homeostasis. The acute post-lesion phase in rats is characterized by adipsia, the lack of an appropriate antidiuretic response, and plasma vasopressin levels which do not rise. Electron micrographs of the supraoptic nucleus and neural lobe of lesioned adipsic rats suggest no stimulation of biosynthetic activity, and large stores of neurosecretory material in the axon terminals. To directly investigate the status of these neurons, we determined neural lobe vasopressin and oxytocin content and the incorporation of [35S]cysteine into hypothalamic proteins in rats with sham-lesions or lesions of the AV3V after 3 days of adipsia or water deprivation, and in water replete sham-lesioned rats. The results demonstrate that adipsic rats with AV3V lesions have neural lobe vasopressin and oxytocin content equivalent to water-replete sham-lesioned rats. Neural lobe vasopressin and oxytocin levels of water-deprived sham-lesioned rats were significantly below those of all other groups. In addition, this group had a radioactivity incorporation rate into hypothalamic proteins which was two-fold greater than either of the other groups. The results indicate that 3-day adipsic AV3V-lesioned rats do not increase neurohypophyseal hormone release or biosynthesis as do 3-day water-deprived sham-lesioned rats. The periventricular tissue of the AV3V would therefore appear to be crucial in providing information to the hypothalamo-neurohypophyseal neurons on body fluid homeostasis.
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PMID:Neurohypophyseal hormone release and biosynthesis in rats with lesions of the anteroventral third ventricle (AV3V) region. 374 94

The anteroventral third ventricle (AV3V) region plays an important role in fluid and electrolyte balance and cardiovascular control in the rat; however, experiments in other species have raised questions about the universality of findings in the rat. The effects of discrete lesions placed within the AV3V area on hydromineral balance, the pressor response to angiotensin II given intravenously, and the initiation of a renin-dependent model of hypertension were examined in the dog. A transpharyngeal approach to the optic chiasm enabled us to destroy only the anterior aspects of the AV3V region (aAV3V group) or to include the entire nucleus medianus (NM) as well (aAV3V + NM group). Lesions of the aAV3V caused polydipsia and transient hypernatremia and hyperosmolality. In contrast, adipsia and a sustained increase in plasma sodium levels and osmolality were observed in dogs with lesions of the aAV3V plus the entire NM. Neither lesion altered baseline arterial pressure, heart rate, plasma levels of catecholamines and vasopressin, or total plasma protein levels. Only in aAV3V + NM lesioned dogs was there a tendency for plasma angiotensin II immunoreactivity to be elevated above control values at 2 and 4 days after operation. Neither lesion attenuated the pressor response to intravenous angiotension II or the initiation of renal hypertension induced by aortic coarctation. As observed in other species, structures within the AV3V region participate in hydromineral balance in the dog; however, in the dog portions of the NM dorsal to the AV3V region are essential for the mediation of drinking behavior.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The anteroventral third ventricle region. Participation in the regulation of blood pressure in conscious dogs. 399 35

Lesions of the tissue surrounding the preoptic recess (AV3V region) have severe effects on body fluid homeostasis; these include acute adipsia and failure of the antidiuretic response. Because neurosecretory cells in supraoptic nuclei comprise the major source of antidiuretic hormone (ADH) in this species, we have previously observed the fine structure of supraoptic nuclei in rats with AV3V lesions. Paraventricular nuclei are the other major source of ADH in rats. Therefore, in this investigation we compared the fine structure of paraventricular nuclei in rats which had received AV3V lesions 3 days earlier with that of control rats which had received sham lesions and either had drinking water available or had water withheld for 3 days. Degenerating axons and axon terminals were present in paraventricular nuclei of lesioned rats. The degenerating terminals were in axodendritic and less often in axosomatic synapses. Morphometric evaluation revealed that neurosecretory cells did respond to the dehydrated state of the adipsic-lesioned animals, but the response was significantly attenuated compared to that which occurred in sham-lesioned rats deprived of water for 3 days. It appears that AV3V lesions damage afferent connections and impair the response of neurosecretory cells to dehydration in paraventricular as well as supraoptic nuclei. However, in paraventricular nuclei the response is not completely prevented by AV3V lesions during the adipsic period as was observed in supraoptic nuclei. The presence of a response in paraventricular nuclei may be at least partially stimulated by reduced body fluid volume. Information from volume receptors would be carried from the medulla to paraventricular nuclei by ascending pathways which are not affected by AV3V lesions.
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PMID:Lesions of the tissue surrounding the preoptic recess (AV3V region) affect neurosecretory cells in the paraventricular nuclei in the rat. 402 71

Here we have reviewed mainly the cerebral regulation of water intake and its relationship with the regulation of the water-retaining antidiuretic hormone (ADH). Much new information of obvious interest has been gained by experiments in conscious animals, by studies in healthy humans, and by clinical investigations. Of particularly great value has been the development of a sensitive radioimmunoassay for determination of plasma ADH (59). The sketchy picture that emerges in light of this new information is as follows. The osmotic regulation of water intake and ADH secretion is exerted by juxtacerebroventricular sensors apparently mainly located on the anterior border of the third ventricle. These sensors may be accessible both to CSF-borne and blood-borne stimuli and inhibitors, and their activity seems to be correlated to the Na concentration of the ECF rather than to its tonicity. A less sensitive volume regulation of water intake and ADH secretion is effectuated by cardiovascular distention and pressure receptors monitoring the effective circulating blood volume, and in severe volume depletion states also by the renin-angiotensin system (RAS). Afferent impulses from the cardiovascular receptors exert a tonic inhibition of the ADH release by acting upon its final neuronal link (the cells of the supraoptic and paraventricular nuclei). Afferent inflow from these receptors also inhibits thirst to some extent, perhaps by preventing at some synaptic level information from cerebral "thirst" sensors from reaching other parts of the brain where the information is converted into a conscious urge to drink. Therefore, increased cardiovascular receptor activity becomes manifested as elevated osmotic thresholds for ADH liberation and thirst. Severe volume depletion may induce RAS hyperactivity to such an extent that generated angiotensin II stimulates the ADH release and water intake. Demonstrated cerebral Na/angiotensin interaction suggests that this may occur via an angiotensin-induced lowering of the stimulus threshold for the sensors involved in the osmotic control of water balance. Cerebral damage affecting the sensors responsible for the osmotic regulation of water intake and ADH release may result in hypo- or adipsia associated with latent diabetes insipidus, and is apparently the ultimate cause of "essential" hypernatremia. This fragmentary outline of the cerebral control of water intake is based to a considerable extent upon circumstantial evidence, and is for that reason speculative on many points.
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PMID:Regulation of water intake. 676 37

Small lesions of the tissue surrounding the anterior ventral third ventricle (AV3V) cause adipsia, but there is no compensatory antidiuretic response. Therefore, the fine structure of the supraoptic nucleus and neural lobe, the major sites of synthesis and release of antidiuretic hormone (ADH), were compared in rats rendered adipsic by AV3V lesions 3 days earlier, rats deprived of water for 3 days and rats drinking normally. In sham-lesioned rats which were deprived of water, neuronal somas in the supraoptic nucleus show signs of stimulated secretory activity. However, the neuronal somas of supraoptic nuclei of rats which did not drink because they were made adipsic by AV3V lesions resemble those of normally hydrated controls. Neural lobes of water deprived animals contain a sharply reduced number of neurosecretory granulated vesicles and reduced apposition of glial processes with the perivascular connective tissue compared to those of normally hydrated rats. In contrast, neural lobes of rats with AV3V lesions contain large accumulations of densely packed neurosecretory vesicles, as well as abundant dense bodies and multilamellar bodies which may be evidence of increased crinophagy, and they have increased interposition of glial processes between axon endings and the perivascular connective tissue. In rats with AV3V lesions the severe dehydration due to adipsia was unable to stimulate release of ADH. The accumulation of neurosecretory vesicles in the neural lobe indicates that transport of ADH to the neural lobe was not impaired in this time period, but that exocytosis of ADH-containing neurosecretory vesicles in the neural lobe was blocked.
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PMID:Ultrastructural effects of anteroventral third ventricle lesions on supraoptic nuclei and neural lobes of rats. 727 46


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