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)

Neurosecretory vesicles of paraventricular corticotropin releasing factor (CRF) neurons increase in size after adrenalectomy (ADX) in parallel with an augmentation of their content in vasopressin (VP) immunoreactive sites. We have investigated in the Brattleboro rat model whether changes in vesicle size are related to elevated intravesicular concentrations of VP. Using quantitative immunoelectron microscopy, VP and CRF immunoreactive sites were assessed in the dense core vesicle compartment of CRF axon terminals in the median eminence. In heterozygous (control) rats, CRF was co-packaged with VP, and ADX induced a 3-fold increase in VP labeling intensity and produced a significant increase in the vesicle diameter. In homozygous rats lacking VP, only CRF immunoreactivity was detectable, and ADX was not accompanied by an increase in vesicle size. These observations suggest that the presence of VP is necessary for the ADX induced increase in vesicle size and that this increase might be needed to accommodate the excess of VP in the vesicle space.
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PMID:The CRF neurosecretory vesicle: vasopressin-dependent changes in vesicle size after adrenalectomy. 147 8

We previously reported that food deprivation significantly decreased arginine-vasopressin (AVP) mRNA levels in the supraoptic (SON) and paraventricular (PVN) nuclei of the hypothalamus and also greatly stimulated the pituitary-adrenocortical system in rats. In this study, we deprived adrenalectomized rats with subcutaneously implanted low-dose corticosterone pellets (ADX + B) of food for 3 days to investigate the involvement of corticosteroid feedback regulation in the food deprivation-induced decrease in AVP mRNA in both the SON and the PVN. The plasma corticosterone levels in these animals were maintained at low levels constantly over 24 h. The ACTH concentration in the morning plasma was markedly increased in the food-deprived ADX + B rats as compared to the fed ADX + B rats. Food deprivation significantly decreased the corticotropin-releasing hormone (CRH) content in the median eminence and increased the CRH and AVP content in the neurointermediate lobe of the pituitary. Semiquantitative in situ hybridization histochemistry revealed that AVP mRNA levels were decreased in the SON but, inversely, increased in magnocellular as well as parvocellular subdivisions of the PVN following food deprivation. These results suggest that: (1) AVP mRNA responds differently to food deprivation between the SON and the PVN; (2) the glucocorticoid feedback can exert on AVP mRNA in the PVN but not in the SON in the food-deprived rats; and (3) food deprivation affects the neurohypophysial levels of CRH and AVP.
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PMID:The magnocellular arginine-vasopressin mRNA responds differently to food deprivation between the supraoptic and paraventricular nuclei of the hypothalamus in adrenalectomized rats with low corticosterone replacement. 150 43

Bilateral adrenalectomy (ADX) leads to increased ACTH synthesis and secretion. It is thought that endogenous glucocorticoids exert a feedback mechanism at both pituitary and brain levels. The present study has been performed in order to determine the effect of ADX on the release of hypothalamic neuropeptides with corticotropin-releasing activity (CRA) and if there exists a median eminence site of glucocorticoid action to regulate hypothalamic-pituitary-adrenal (HPA) function. Adrenalectomized and sham-operated male rats were killed at different periods after surgery (2, 5, 7 and 14 days) and trunk blood was collected for ACTH and corticosterone (B) concentrations measurement. Brain (median eminence, ME; and medial basal hypothalamus, MBH) and pituitary (anterior lobe, AP; and neurointermediate lobe, NIL) tissues were dissected in order to evaluate either peptide content or in vitro hormone release. The results indicate that ADX blunted plasma B levels and increased AP ACTH content and secretion in a time-related fashion up to the 14th day. ADX significantly decreased both CRF and CRA contents in the ME at all periods studied; ME arginine-vasopressin (AVP) increased 7 and 14 days after ADX. MBH CRF decreased after ADX, but returned to sham value 2 weeks later; similarly, MBH AVP decreased at all periods after ADX. Removal of endogenous glucocorticoids did not vary neither oxytocin (OXY) content in the ME and MBH nor AVP and OXY contents in the NIL. In our superfusion experiments, we found that ADX increased basal AVP release and did not change spontaneous CRF secretion from ME terminals. Dexamethasone (Dxm, 10 nM) diminished AVP but not CRF output by ME tissues from adrenalectomized rats. A direct relationship was found between ME CRF and 28 mM KCl (hK+)-induced CRF release by MEs from adrenalectomized rats. ME fragments from adrenalectomized rats were hyperresponsive to kH+ stimulation of AVP release. Dxm (10 nM) decreased the hK(+)-evoked CRF and AVP release by MEs from adrenalectomized rats. ADX and dexamethasone treatment did not influence basal and hK(+)-elicited ME OXY release. Additionally, a rapid glucocorticoid inhibitory effect on ACTH secretion by isolated AP cells from both sham and adrenalectomized rats was found, and an in vitro corticotrope hyporesponse to 0.63 nM CRF and 9.25 nM AVP stimulation during several days after ADX.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Changes in the hypothalamo-corticotrope axis after bilateral adrenalectomy: evidence for a median eminence site of glucocorticoid action. 184 20

To identify brain sites responding to the removal of corticosterone feedback by adrenalectomy (ADX), rat brains were processed for fos immunocytochemistry 1, 3, and 7 days after ADX, sham-ADX, or no surgery using a polyclonal antiserum to fos residues 132-154. Compared to SHAM, ADX rats exhibited strong fos-like immunoreactivity (FLI) only in the parvocellular neurons of the paraventricular hypothalamic nuclei (PVN) 1, 3, and 7 days after surgery. Replacement with a corticosterone pellet at the time of adrenalectomy (ADX + B) prevented this increase in PVN FLI in three of four rats at 1 day, all rats at 3 days, and two of seven rats 7 days after surgery; 100 micrograms/ml corticosterone in the drinking water for 2 days before perfusion reversed ADX-induced increases in PVN FLI in 7-day ADX rats. Providing 25 micrograms/ml corticosterone in the drinking water to ADX rats for 5 days after surgery did not prevent expression of PVN FLI, even though this dose has been shown to normalize morning basal ACTH levels in ADX rats. Virtually all parvocellular PVN neurons expressing FLI after ADX costained for CRF. Some parvocellular neurons also expressed both fos and vasopressin. In all rats, many brain regions expressed FLI that was not related to adrenalectomy. We conclude that the changes in neuronal FLI correlate with demonstrated changes in neuroendocrine activity after ADX; however, suppression of ADX-induced FLI may require higher replacement levels of corticosterone than inhibition of ADX-induced ACTH secretion.
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PMID:Induction of fos-like immunoreactivity in hypothalamic corticotropin-releasing factor neurons after adrenalectomy in the rat. 215 9

Male Wistar rats were anaesthetized, injected intracisternally (i.c.) with saline or colchicine and were decapitated at various time intervals. Trunk blood was collected for the determination of immunoreactive adrenocorticotropic hormone (ACTHi) by radioimmunoassay (RIA) and of corticosterone by a fluorometric assay. Changes in corticotropin-releasing factor (CRF) content of the median eminence (ME) were assessed by quantitative immunocytochemistry (QICC) on cryostat sections of ME preparations or by RIA of CRF in ME-extracts. Administration of colchicine resulted in a long-lasting and dose-dependent stimulation of ACTHi secretion. At a dose of 25 micrograms, high plasma ACTHi levels were found for up to 24 h. A dose of 5 micrograms per rat, that has been reported to effectively block vasopressin transport in paraventricular-neurohypophyseal neurons, resulted in a small elevation of plasma ACTHi. In intact rats, i.c. administration of saline of saline containing 5 micrograms of colchicine had no effect on the CRF content in the ME. In contrast, colchicine caused a depletion of the CRF stores in the ME of 1-week adrenalectomized (ADX) rats. The disappearance rate was 9.2%/h as measured by RIA and 11.2%/h as measured by QICC. When plasma corticosterone and ACTHi were normalized by giving ADX rats corticosterone in drinking water, the colchicine-induced depletion of the CRF stores was fully prevented. We conclude that the rate of decline of CRF in the ME of rats treated with a non-toxic dose of colchicine to block axonal transport is positively correlated to the secretory activity of CRF neurons of the paraventricular-infundibular system.
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PMID:Effect of axonal transport blockade on corticotropin-releasing factor immunoreactivity in the median eminence of intact and adrenalectomized rats: relationship between depletion rate and secretory activity. 245 50

In the present study we report the properties of vasopressin (VP) receptors in the anterior pituitary gland and show that the number of these receptors is markedly affected by adrenalectomy and hypothalamic lesions. VP-binding activity was assayed in particulate fractions of rat anterior pituitary glands using tritium-labeled arginine VP ([3H] AVP) as tracer. In the presence of Mg2+ the radioligand interacted with a single class of high affinity, low capacity binding sites. Magnesium ions modulated the affinity of the receptors but had no effect on binding capacity. Guanine nucleotides decreased the amount of tracer bound in a dose-dependent manner by increasing the dissociation constant (Kd) of the binding reaction by approximately 2-fold. Increasing the concentration of Mg2+ did not prevent this effect. Bilateral adrenalectomy (ADX) decreased pituitary AVP-binding activity: binding fell by 30% 4 h after surgery and declined further to 10% or less of control at 4 days. The decrease in binding was primarily due to a reduction in the number of receptors. Daily administration of corticosterone inhibited the reduction of binding activity at 4 days in a dose-dependent manner. Destruction of hypophyseotropic VP neurons by means of surgical lesioning of the hypothalamic paraventricular nucleus or the medial basal hypothalamus abolished the effect of ADX on pituitary AVP binding at 24 h but only attenuated the degree of receptor loss at 4 days. Furthermore, the lesions themselves caused a significant (approximately 30%) reduction in receptor number 4-7 days after hypothalamic surgery. Adrenalectomy reduced pituitary AVP-binding activity in homozygous (di/di) Brattleboro rats. The extent as well as the time course of the loss of receptor activity resembled that in normal rats. Rat anterior pituitary segments were exposed to synthetic CRF, AVP, or oxytocin (all 10(-7) M) for 4 h in vitro, and [3H] AVP-binding activity was subsequently determined. Both AVP and oxytocin reduced the amount of radioligand bound, while CRF had no effect. These observations allow the following conclusions: Magnesium ions and guanine nucleotides modulate the affinity of pituitary AVP receptors by different mechanisms and have no effect on binding capacity; Pituitary receptors for AVP are regulated by the amount of AVP released by paraventricular nucleus neurons as well as through a mechanism that requires the presence of corticosterone; Homozygous Brattleboro rats may respond to ADX by increased hypothalamic release of an endogenous ligand for pituitary AVP receptors.
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PMID:Pituitary binding of vasopressin is altered by experimental manipulations of the hypothalamo-pituitary-adrenocortical axis in normal as well as homozygous (di/di) Brattleboro rats. 316 22

Many parvocellular neurons in the paraventricular nucleus of the hypothalamus express high levels of corticotropin releasing factor (CRF) or vasopressin following adrenalectomy. To determine whether glucocorticoids feed back directly on these neurons, a mouse monoclonal antibody directed against the rat liver glucocorticoid receptor was used in combination with polyclonal antisera directed against either vasopressin or CRF to permit simultaneous visualization of either peptide with glucocorticoid receptor-like immunoreactivity (IR). Rats were adrenalectomized (ADX) for 2 weeks to optimize numbers of vasopressin - and CRF-IR neurons. Six hours prior to sacrifice, a separate group of adrenalectomized rats was treated with corticosterone (40 mg/kg). This short-term replacement resulted in nuclear localization of glucocorticoid receptor-like-IR but did not attenuate the increased numbers of CRF- and vasopressin-IR neurons observed after adrenalectomy. It was therefore possible to visualize vasopressin- or CFR-IR and nuclear glucocorticoid receptor-like-IR simultaneously. Cell counts of double-labeled neurons in the paraventricular nucleus of the hypothalamus (PVH) demonstrated that glucocorticoid receptor-like-IR is colocalized in virtually all the CRF and vasopressin immunoreactive parvocellular neurons studied, which respond to adrenalectomy by increased peptide expression. These data suggest that a major feedback effect of glucocorticoids on the hypothalamic-pituitary-adrenal axis is exerted directly within nuclei of CRF and vasopressin neurons.
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PMID:Demonstration of glucocorticoid receptor-like immunoreactivity in glucocorticoid-sensitive vasopressin and corticotropin-releasing factor neurons in the hypothalamic paraventricular nucleus. 326 Feb 89

A combined retrograde transport-immunohistochemical method was used to compare the numbers of corticotropin-releasing factor (CRF) and vasopressin-immunoreactive neurons in the paraventricular nucleus of the hypothalamus (PVH) that could be retrogradely labeled after tracer injections in the dorsomedial medulla or the spinal cord in untreated, colchicine-treated, and adrenalectomized (ADX) male rats. In untreated animals, very few CRF-stained cells were retrogradely labeled after tracer injections in either target, while a modest number, comparable to that seen in previous studies, of vasopressinergic cells were found to project to one or both structures. Animals pretreated with colchicine, a non-specific inhibitor of axonal transport, displayed CRF immunoreactivity in a small percentage of retrogradely labeled neurons in the PVH; the number of retrogradely labeled vasopressin-immunoreactive cells was comparable to that seen in untreated rats. Despite the fact that ADX animals displayed enhanced immunostaining for both peptides in the parvocellular division of the PVH, the number of retrogradely labeled cells stained for each peptide was similar to that seen in controls. The results establish that CRF is contained within the long descending projections of the PVH, and are consistent with the view that adrenal steroid withdrawal preferentially enhances the expression of CRF and vasopressin in parvocellular neurosecretory neurons.
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PMID:Evidence for differential regulation of corticotropin-releasing factor and vasopressin immunoreactivities in parvocellular neurosecretory and autonomic-related projections of the paraventricular nucleus. 332 30

CRF-containing parvocellular axons in the external zone of the rat median eminence were classified as vasopressin-containing (CRF+/AVP+) and vasopressin-deficient (CRF+/AVP-) subpopulations based on post-embedding electron microscopic immunocytochemical staining of serial ultrathin sections for CRF, AVP and the other peptides derived from the AVP precursor: AVP-associated neurophysin (NP-AVP) and the C-terminal glycopeptide (GP). In normal animals, the CRF+/AVP+ and CRF+/AVP- subpopulations were approximately equal in terms of detectable axonal swellings. Three to 14 days after adrenalectomy (ADX), the CRF+/AVP+ and CRF+/AVP- subpopulations represented about 95% and 5%, respectively, of total CRF+ swellings. This change was due to a 90% decrease in the absolute number of detectable CRF+/AVP- swellings after ADX, whereas the absolute number of detectable CRF+/AVP+ swellings rose by less than 20%. These changes were completely blocked by administering the glucocorticoid agonist dexamethasone throughout the period after ADX. The results suggest that the CRF+/AVP+ and CRF+/AVP- subpopulations of neurosecretory axons in the external zone of the median eminence respond differently to ADX, indicating that they are independently regulated by glucocorticoids.
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PMID:Vasopressin-containing and vasopressin-deficient subpopulations of corticotropin-releasing factor axons are differentially affected by adrenalectomy. 349 95

The separate role of mineralocorticoid and glucocorticoid hormone action in maintaining arterial pressure was studied in normotensive rats. Four groups were prepared: adrenalectomized (ADX) rats given 6 micrograms aldosterone/24 h (ALDO; n = 9) or 10 micrograms dexamethasone/24 h (DEX; n = 9) by intraperitoneal Alzet pumps, shamoperated controls (control; n = 10) and ADX rats with no hormone replacement (ADX; n = 9). All groups were given 1% NaCl + 2.5% glucose drinking solution. Measurements of plasma corticosterone and aldosterone and urinary aldosterone excretion confirmed the adequacy of the experimental groups. Forty-eight hours after ADX or sham, base-line intra-arterial mean arterial pressure (MAP) in conscious undisturbed rats was similar in the four groups. Captopril (1 mg/kg iv) produced a similar reduction in MAP in ALDO (-11 +/- 2 mmHg) and DEX (-12 +/- 1 mmHg) groups, despite a lower plasma renin activity (PRA) in ALDO (2.0 +/- 0.7 and 6.0 +/- 1.5 ng X ml-1 X h-1, respectively; P less than 0.05). dP (Me)TyrAVP (50 micrograms/kg iv) caused a greater decrease in MAP in ALDO (-15 +/- 3 mmHg) than in DEX (-8 +/- 1 mmHg; P less than 0.05). Combined blockade with both antagonists resulted in a greater MAP reduction in ALDO (-29 +/- 4 mmHg) than in DEX (-15 +/- 4 mmHg; P less than 0.05). These results indicate that glucocorticoid hormone action maintains arterial pressure in ADX rats by mechanisms similar to normal rats and largely independent of the renin-angiotensin system and vasopressin. In contrast, mineralocorticoid replacement alone in ADX rats requires increased participation of both peptide systems for maintenance of arterial pressure.
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PMID:Role of mineralocorticoids and glucocorticoids in blood pressure regulation in normotensive rats. 353 7


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