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)

Fetal hypothalami obtained from normal Long-Evans rats were transplanted to the lateral, third or fourth ventricle of adult male Brattleboro rats, homozygous for diabetes insipidus. The density of the capillary plexuses within the grafts did not vary as a function of their intraventricular location; all transplants exhibited a capillary density equivalent to that of the in situ hypothalamus. Intravascular injections of HRP resulted in retrograde neuronal labeling only in grafts that were attached to circumventricular organs of the host brain, especially the median eminence. Typically, HRP-associated label was confined to vascular and perivascular elements and not diffusely distributed within the graft parenchyma, indicating that capillaries within the transplants developed barrier properties similar to those of the native hypothalamus. Neural integration of the transplant with the recipient brain was limited; at most points of apposition the neuropil of graft and host were separated by an intervening ependymal layer or glia limitans. All surviving grafts contained neurophysin and/or vasopressin-immunoreactive (VP-ir) neurons. Three anatomically distinct populations of VP-ir neurons were identified. Magnocellular VP-ir neurons were identified in less than half of the grafts, and when present they were few in number distinct, but sparse vasopressinergic innervation of median eminence capillaries was observed in all cases where grafts containing magnocellular neurons were apposed to this structure. Most grafts contained numerous, parvicellular VP-ir neurons arranged in aggregations which resembled the suprachiasmatic nucleus (SCN). SCN-like cell groups projected to neural targets within the graft and the host brain, but they did not project onto blood vessels. A second, distinct class of parvicellular VP-ir neuron also was identified in a majority of transplants. In contrast to SCN-like ('type' I) cells, these 'type II' parvicellular neurons were somewhat larger and found in less discretely organized groups, and they projected to vascular targets; usually locally elaborated capillary plexuses intrinsic to the transplants. In the present study, there was no amelioration of the symptoms of diabetes insipidus in the host animals despite the presence of numerous VP-ir neurons in virtually all grafts. This was probably related to the limited survival of magnocellular VP-ir neurons, which appear to be the principal source of vasopressinergic projections from the graft to fenestrated capillary plexuses of the host brain.
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PMID:Characteristics of vasculature and neurovascular relations in intraventricular anterior hypothalamic transplants. 244 72

In situ hybridization, Northern blotting, and solution hybridization assay were used to examine vasopressin-gene messenger ribonucleic acid (mRNA) transcripts in hypothalamic tissue from five strains of rats: Long-Evans, Wistar-Kyoto, and diabetes insipidus (Brattleboro) rats, spontaneously hypertensive-stroke-prone rats, and cross-bred diabetes insipidus x spontaneously hypertensive-stroke-prone rats. A 290 base-pair, single-stranded RNA probe, with 221 bases complementary to exon C of the vasopressin gene was synthesized by the SP6 transcription vector system. This probe labeled appropriate neurohypophysial hypothalamic neurons, as well as suprachiasmatic nucleus cells, in tissue samples from all five strains of rats. Confirming other recent hybridization results with diabetes insipidus rat brain tissue, diabetic animals were found to transcribe their mutated vasopressin gene. In addition, this investigation found that the cross-bred diabetic-hypertensive rat also synthesizes a vasopressin-gene messenger ribonucleic acid transcript. Quantitative analyses of solution and in situ hybridization results suggested the cross-bred diabetic-hypertensive rat exhibits a level of vasopressin-gene messenger ribonucleic acid similar to diabetes insipidus rats. This observation is consistent with previous data on the cross-bred diabetic-hypertensive rat which suggests they inherit the mutant vasopressin gene from Brattleboro rats.
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PMID:In situ hybridization demonstrates vasopressin gene transcription in hypothalamic neurons of crossbred hypertensive x diabetes insipidus rats. 246 87

1. Plasma volumes and cardiovascular status were assessed in rats with a congenital deficiency in hypothalamic vasopressin (Brattleboro strain) and in the parent strain (Long Evans), in water-replete and water-deprived states. 2. Water-replete Brattleboro rats were not hypovolaemic; water deprivation (14 h in Brattleboro rats, 53 h in Long Evans rats) produced similar percentage reductions in plasma volumes in the two groups. 3. In the water-replete state, cardiovascular variables were similar in Long Evans and Brattleboro rats. Inhibition of ganglionic transmission (with pentolinium) or of the renin-angiotensin system (with captopril), separately, did not have a greater effect on blood pressure in Brattleboro rats than in Long Evans rats. Recovery from hypotension caused by pentolinium was characterized by large swings in blood pressure in both groups of rats. These pressor episodes were abolished by administration of captopril to Brattleboro rats. After administration of pentolinium and captopril to Long Evans rats there was a substantial, although intermittent, recovery in blood pressure that was abolished by an antagonist of the cardiovascular actions of vasopressin. 4. In the water-deprived state, blood pressures were similar in Long Evans and Brattleboro rats; both groups showed an elevation in diastolic blood pressure relative to the water-replete state. After administration of pentolinium, there was a more marked recovery in blood pressure than was seen in the water-replete state. Administration of captopril alone had a slightly greater effect on blood pressure in Long Evans rats in the water-deprived, compared with the water-replete, state. However, in the former condition, Brattleboro rats showed a profound and progressive hypotension in response to captopril, indicating an indispensable role for the renin-angiotensin system in the maintenance of blood pressure in these animals during water deprivation. 5. Only when the renin-angiotensin system and neural activity were inhibited did vasopressin express its full, independent, pressor potential in Long Evans rats. However, evidence was obtained that vasopressin may exert important effects on cardiovascular regulation via neural mechanisms and through interactions with the renin-angiotensin system.
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PMID:Interactions between neural mechanisms, the renin-angiotensin system and vasopressin in the maintenance of blood pressure during water deprivation: studies in Long Evans and Brattleboro rats. 248 66

1. The cardiovascular effects of bolus intravenous injections of vasopressin, angiotensin II and noradrenaline were studied in 6-hydroxydopamine pretreated, anaesthetized Brattleboro rats with hereditary diabetes insipidus and normal rats of the parent Long Evans strain. 2. Pretreatment with 6-hydroxydopamine did not significantly affect control values for mean arterial blood pressure, cardiac output or total peripheral resistance in either Brattleboro or Long Evans rats but the pressor response to haemorrhage was reduced in both strains compared to the control animals. 3. The pressor responses of the untreated Brattleboro rats to 250 mu kg-1 vasopressin were significantly greater and more prolonged than in control rats of the Long Evans strain. 4. Pretreatment with 6-hydroxydopamine significantly enhanced the peak pressor response to vasopressin, but not to angiotensin II (1 microgram kg-1), in Brattleboro and Long Evans rats. 5. Pretreatment with 6-hydroxydopamine resulted in an enhanced pressor response to 1 microgram kg-1 noradrenaline in both Brattleboro and Long Evans rats, but the effect was significantly greater in the vasopressin-deficient animals. 6. These results indicate differences in the pressor responsiveness of Brattleboro rats to vasopressin and noradrenaline, but not to angiotensin II, compared with control Long Evans rats and provide evidence for important interactions between the sympathetic nervous system and these pressor hormones.
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PMID:Cardiovascular interactions between vasopressin, angiotensin and noradrenaline in the Brattleboro rat. 249 61

The effects of arginine vasopressin (AVP), and of the V2-AVP receptor agonist 1-deamino[8-D-arginine] vasopressin (DDAVP) on release from the vasopressin-neurons and oxytocin-neurons of Long-Evans rats were evaluated using specific radioimmunoassays for rat neurophysins. AVP (1 microgram, 1 nmol) or DDAVP (25 ng, 25 pmol) was administered i.p. to animals 1 h before they received an i.v. infusion of 18% saline at 10 microliters/100 g b. wt./min for 60 min. Both AVP and DDAVP decreased the responsiveness (slope) but not the sensitivity threshold of vasopressin-neurons to acute changes in plasma osmolality. Since the amounts of the peptides giving comparable decreases in responsiveness were directly related to their antidiuretic potencies, it is most probable that this influence is mediated through V2-like receptors. However, while ruling out a significant contribution of V1-type receptors, the data do not exclude involvement of other vasopressin receptors (e.g. V3-type receptors). Both AVP and DDAVP also appeared to have an inhibitory effect on release from oxytocin-neurons, but in this case they significantly altered sensitivity threshold but not responsiveness to acute changes in plasma osmolality. Because AVP produced a shift in sensitivity threshold larger than that by DDAVP when the peptides were used in amounts related to their antidiuretic potencies, our results suggest that the feedback influence of AVP on oxytocin-neurons is largely, although not entirely, exercised through V2-like receptors.
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PMID:Vasopressin reduces release from vasopressin-neurons and oxytocin-neurons by acting on V2-like receptors. 252 39

To evaluate the role of vasopressin in the regulation of atrial natriuretic peptide (ANP) secretion, the plasma, atrial, ventricular, and hypothalamic levels of ANP were measured in Long-Evans (LE) and vasopressin-deficient Brattleboro (DI) rats. Total atrial immunoreactive ANP (IR-ANP) as well as right auricular IR-ANP concentration were higher in the DI than in the LE rats, whereas no significant difference was noted in left auricular IR-ANP concentration. In the left ventricle of DI rats, the IR-ANP concentration was 82% greater than that in the LE rats, while no substantial difference was found in the right ventricular IR-ANP concentration between the strains. Normal LE rats had low levels of left ventricular ANP mRNA and barely detectable ANP mRNA in the right ventricle, DI rats showed a 3-fold greater ANP mRNA concentration in the left ventricle than age-matched LE controls, and ANP mRNA levels were also increased in the left auricle of DI rats. The hypothalamic IR-ANP content, but not the concentration, was significantly increased in the DI compared to the LE rats. Despite increased cardiac IR-ANP and ANP mRNA levels, plasma IR-ANP concentrations were similar in the conscious DI rats (97 +/- 9 pg/ml; n = 13) and the LE rats (95 +/- 8 pg/ml; n = 15). Volume expansion (1.1 ml/100 g BW of 0.9% saline, iv) increased right atrial pressure and caused a significant rise in plasma IR-ANP in both strains (P less than 0.01). Elevations of plasma IR-ANP concentrations caused by volume loading were comparable in LE and DI rats in either the absence or presence of exogenous vasopressin (5 ng/kg.min, iv), which, when infused alone, did not significantly influence the plasma IR-ANP concentration. However, the relation between the change in IR-ANP concentration and the change in right atrial pressure shifted to the left, and thus, for a given increase in right atrial pressure, a greater amount of IR-ANP was released in the vasopressin-treated rats than in the control animals. These results demonstrate that although acute volume expansion does not necessarily require endogenous vasopressin for the ANP secretory response, vasopressin increased the ability of volume expansion to induce ANP release, thus modulating the direct mechanical stimulus-induced ANP secretion. The increased left ventricular levels of immunoreactive ANP and augmentation of ANP mRNA levels in Brattleboro rats despite normal left ventricular weight to body weight ratio show that increased ANP gene expression may occur in the ventricles independently of hypertrophy.
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PMID:Atrial natriuretic peptide in plasma, atria, ventricles, and hypothalamus of Long-Evans and vasopressin-deficient Brattleboro rats. 252 4

Young, conscious Long-Evans rats had significantly higher basal mean arterial blood pressure than age-matched Brattleboro rats with hereditary hypothalamic diabetes insipidus, and an intravenous injection of a specific vasopressin V1-receptor blocker significantly decreased the mean arterial pressure in the former animals only. The basal heart rate, which was significantly higher in the Brattleboro rats than in the Long-Evans rats, was unaffected by the vasopressin antagonist in either strain. These results indicate that vasopressin may be important in maintaining normal blood pressure in young rats.
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PMID:Vasopressin V1-receptor blockade lowers arterial blood pressure in young conscious Long-Evans rats. 252 46

Previous studies suggest that circulating levels of vasopressin (AVP) influence the responsiveness of the kidney to AVP. To determine how changes in renal AVP receptors and adenylate cyclase (AC) contribute to such altered responsiveness, we analyzed AVP receptors and AVP-sensitive AC in kidneys from Sprague-Dawley, Long-Evans and homozygous Brattleboro rats. In autoradiographic studies, the distribution of [3H]AVP binding sites was similar in all groups, corresponding to the location of AVP-sensitive AC: collecting ducts greater than outer medullary collecting ducts greater than medullary thick ascending limb greater than cortical collecting ducts. No differences in AVP receptor affinity or content were observed in kidney medullary membranes from Sprague-Dawley, Long-Evans or Brattleboro rats (KD = 0.8, 0.9, and 0.7 nM; Bmax = 116 +/- 9, 95 +/- 11 and 98 +/- 6 fmol/mg). Basal and AVP-stimulated AC activities were lower in kidney membranes from Brattleboro rats compared with Sprague-Dawley and Long-Evans animals (basal = 28 +/- 4, 40 +/- 4 and 38 +/- 3 pmol cAMP/mg/min; EDmax = 57 +/- 5, 80 +/- 7 and 71 +/- 2 pmol cAMP/mg/min) with no change in ED50. In 48-hour water-deprived Sprague-Dawley rats, AVP receptors were decreased from 116 +/- 9 to 58 +/- 2 fmol/mg, suggesting that AVP receptors are down-regulated by elevated AVP blood levels. The absence of changes in basal or AVP-stimulated AC in dehydrated rats indicates that receptor-AC coupling is normal and that maximum AC activation can occur with partial receptor occupancy. The data also indicate that impaired renal responsiveness to AVP in Brattleboro rats is not due to down-regulation of AVP receptors.
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PMID:Physiologic regulation and distribution of the renal vasopressin receptor. 253 25

In brain slices of normal Wistar and Long-Evans rats, brief high frequency stimulation of the fimbria fibers induced long-term potentiation (LTP) in excitatory transmission between these fimbria fibers and neurons of the lateral septum (LS). Slices prepared from diabetes insipidus (DI) Brattleboro rats, that contained no vasopressin (VP), consistently failed to maintain LTP in this excitatory transmission. Exogenous VP, administered to slices from DI Brattleboro rats shortly prior to the experiment or released from a subcutaneous depot in DI Brattleboro rats for several days prior to decapitation, corrected this failure. The maintenance of LTP in the LS in slices from Wistar and Long-Evans rats was prevented by D(CH2)5-Tyr(Me)-arginine VP, an antagonist for the V1 type of VP receptors. These results indicate an important role of VP in the maintenance of LTP in excitatory transmission in the LS. It is conjectured that the effects of VP on LS neurons are related to the role of the peptide in the maintenance of LTP and that these processes play a role in memory formation.
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PMID:Vasopressin maintains long-term potentiation in rat lateral septum slices. 253 55

The cardiovascular effects of noradrenaline injected into the hypothalamic paraventricular nucleus (PVN) were investigated in conscious Long-Evans (control) rats and homozygous vasopressin (AVP)-deficient Brattleboro rats. Unilateral microinjection of noradrenaline (3-30 nmol) into the PVN produced dose-dependent increases in systolic and diastolic blood pressure of Long-Evans rats, and a concomitant decrease in heart rate. Only the highest dose of noradrenaline tested (30 nmol) caused a significant pressor response in Brattleboro rats (9 +/- 4/9 +/- 4 mm Hg, systolic/diastolic, n = 7) which was significantly smaller than the response produced by the same dose of noradrenaline in Long-Evans rats (32 +/- 8/27 +/- 6 mm Hg, n = 7). Intravenous pretreatment of Long-Evans rats with the V1-receptor antagonist, d(CH2)5Tyr[Et]DAVP, almost completely abolished the pressor effect of noradrenaline (10 nmol) without significantly attenuating the bradycardia. The alpha 2-adrenoceptor antagonist, idazoxan (4 nmol), injected into the PVN abolished the pressor response produced by noradrenaline (10 nmol) in Long-Evans rats but had no significant effect on the bradycardia. Pretreatment with the alpha 1-adrenoceptor antagonist, prazosin (0.7 nmol), significantly attenuated both the pressor and bradycardic effects of noradrenaline in Long-Evans rats. These results suggest that the pressor response produced by microinjection of noradrenaline into the hypothalamic PVN of conscious Long-Evans rats is mediated largely through stimulation of alpha 2-adrenoceptors and is dependent, in part, on release of AVP into the circulation. A component of the bradycardia seen with this intervention may be mediated through stimulation of alpha 1-adrenoceptors in the PVN.
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PMID:Paraventricular nucleus injections of noradrenaline: cardiovascular effects in conscious Long-Evans and Brattleboro rats. 255 99


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