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)

Behavioral stress and high dietary salt have been reported to increase blood pressure additively in non-human primates. This study was designed to replicate this phenomenon and to assess neuroendocrine correlates and responses to two commonly used antihypertensives, a beta-adrenoceptor blocker and a thiazide diuretic. High-salt intake (240 mmol sodium per day) and stress were administered for 9 weeks in adult baboons. Oral atenolol hydrochloride (50 mg, twice daily) or hydrochlorothiazide (25 mg/day) was administered for 2 weeks each. In all four baboons, salt loading and stress increased systolic blood pressure (SBP) chronically by 14 mmHg, with increases in water intake, urine osmolality and excretion of sodium, decreases in levels of serum sodium, plasma renin activity and plasma vasopressin and no changes in urinary excretion of norepinephrine or epinephrine. Neither drug decreased SBP during ongoing high salt and stress. The results confirm the additive chronic effects of high-dietary salt intake and behavioral stress on blood pressure in non-human primates. The hypertension in this model is resistant to two antihypertensive drugs commonly used clinically.
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PMID:Stress and sodium hypertension in baboons: neuroendocrine and pharmacotherapeutic assessments. 165 40

Quantitative autoradiography was used to localize and characterize atrial natriuretic peptide (ANP) receptors in the rat brain and to study their regulation. Peptide receptors are selectively located to circumventricular organs outside the blood brain barrier, such as the subfornical organ, and to brain areas involved in fluid and cardiovascular regulation. Dehydration, either by water deprivation of normal rats, or chronic dehydration present in homozygous Brattleboro rats lacking vasopressin, results in large increases in ANP binding in receptor number in the subfornical organ. In the deoxycorticosterone acetate (DOCA)-salt hypertensive model, only salt treatment, but not DOCA alone or the combination of DOCA-salt, increased the ANP receptor number in the subfornical organ and the choroid plexus. Both young and adult genetically hypertensive rats have a greatly decreased ANP receptor number in the subfornical organ and the choroid plexus. Selective displacement with an inactive analog lacking the disulfide bond (ANP 111-126) suggests that genetically hypertensive rats may lack C (clearance) atrial natriuretic peptide receptors. Our results implicate brain atrial natriuretic peptide receptors in the central response to alterations in fluid regulation and blood pressure.
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PMID:Autoradiography of atrial natriuretic peptide (ANP) receptors in the rat brain. 166 18

Peripheral sympathetic neurons are thought to provide trophic regulatory signals for development of their target tissues. In the current study, we investigated the role of sympathetic tone in the functional development of the kidney in rats, using neonatal intracisternal administration of 6-hydroxydopamine (6-OHDA). This treatment destroys central catecholaminergic pathways and permanently reduces sympathetic activity without ablating peripheral nerve terminals. Renal function was evaluated over the first two postnatal weeks, when glomerular and tubular function undergo rapid development. Although basal renal clearance and the homeostatic response to fluid deprivation developed normally in the lesioned rats, the response to a maximally-effective dose of desmopressin acetate (DDAVP), a vasopressin analog, became deficient by the end of the second week. After weaning, the lesioned animals were unable to survive a chronic salt load, which requires sustained water reabsorption but high output of sodium. These data indicate that normal sympathetic tone is required for appropriate development of the responsiveness of the renal tubule to vasopressin.
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PMID:Neural factors in the development of renal function: effect of neonatal central catecholaminergic lesions with 6-hydroxydopamine. 168 71

In situ hybridization histochemistry and indirect immunofluorescence histochemistry were used to study changes in the expression of vasopressin (VP), oxytocin (OXY), tyrosine hydroxylase (TH), galanin (GAL), dynorphin (DYN) and cholecystokinin (CCK) in hypothalamic magnocellular neurons of the paraventricular (PVN) and supraoptic (SON) nuclei of rats. After prolonged administration of 2% sodium chloride as drinking water (salt-loading), the treatment increased the levels of VP, OXY, TH, GAL, DYN and CCK mRNA in the PVN and SON. The increase in CCK mRNA was, however, proportionally higher in the PVN than in the SON. Within cell bodies of the PVN and SON of salt-loaded rats, a depletion of VP- and OXY-like immunoreactivity (LI) and an increase in TH-LI were seen. In salt-loaded/colchicine-treated rats, a marked decrease in GAL- and DYN-LI, but no specific changes in CCK-LI were observed. Within nerve fibers of the posterior pituitary of salt-loaded rats, a marked depletion of VP-, GAL- and DYN-LI was found. Less pronounced depletion was observed in OXY- and CCK-LI, and no specific changes in TH-LI were seen. The results show that high plasma osmolality induces increased mRNA levels for VP, OXY, TH, GAL, DYN and CCK, presumably indicating increased synthesis, an increased export from cell somata of VP, OXY, GAL and DYN, and a decrease in levels of these peptides in the posterior pituitary, suggesting increased release. The catecholamine-synthesizing enzyme TH, however, which has a cytoplasmic localization and is not released from nerve endings, remains high in the cell bodies and nerve endings during this state of increased activity.
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PMID:Peptides and transmitter enzymes in hypothalamic magnocellular neurons after administration of hyperosmotic stimuli: comparison between messenger RNA and peptide/protein levels. 169 5

The purpose of the present study was to determine whether Ang II releases adenosine from the perfused rat lung. Rat lungs were perfused in situ with a physiological salt solution and were loaded with [3H]adenosine. The release of 3H from the perfused rat lung in response to intra-arterial injections of Ang II and other hormones was quantitated. Studies were conducted in both normal rats and in rats that had been nephrectomized before surgery to avoid exposure of the lungs to high levels of endogenous Ang II. Bolus doses of Ang II (10(-12)-10(-7) mol) increased the efflux of 3H from the lungs. Analysis of this effluent by thin-layer chromatography indicated that most of the Ang II-induced release of 3H was [3H]adenosine. The maximal response was usually obtained with 10(-9) mol, and higher doses (10(-8) and 10(-7) mol) mobilized less [3H]adenosine, which suggested tachyphylaxis. The effect of exogenous Ang II on [3H]adenosine release was greatly enhanced when activation of the endogenous renin-angiotensin system was prevented with prior nephrectomy. Infusion of the Ang II selective antagonist, (1-Sar-8-Ile)-Ang II, blocked Ang II-induced [3H]adenosine release. Neither norepinephrine, bradykinin, nor vasopressin consistently released adenosine. We conclude that (a) Ang II can induce the release of adenosine from the perfused rat lung, (b) this effect is receptor mediated, (c) this response is somewhat selective for Ang II, and (d) exposure to high levels of exogenous or endogenous Ang II causes tachyphylaxis so that Ang II-induced adenosine release is attenuated.
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PMID:Angiotensin II-induced [3H]adenosine release from in situ rat lung. 169 51

Indirect immunofluorescence histochemistry was used to investigate the distribution and extent of co-localization of chemical messengers in magnocellular neurons of the supraoptic and paraventricular nuclei. In order to increase the number of neurons immunoreactive to the antisera used, experimental manipulations were employed. The homozygous Brattleboro (diabetes insipidus) rat was also investigated. In untreated rats, only vasopressin- and oxytocin-like immunoreactivities could be observed. Colchicine treatment alone resulted in appearance of galanin-, dynorphin-, cholecystokinin-, [Leu]enkephalin- and thyrotropin-releasing hormone-positive cells. In hypophysectomized rats, all these markers, except tyrosine hydroxylase, showed substantial further increases. In addition, peptide histidine-isoleucine-immunoreactive cell bodies could now be seen. After salt-loading alone, tyrosine hydroxylase-like immunoreactivity was markedly increased, whereas vasopressin- and oxytocin-like immunoreactivity were very weak or undetectable. When salt-loaded rats received colchicine, corticotropin-releasing factor- and peptide histidine-isoleucine-like immunoreactivity in addition increased, whereas galanin- and dynorphin-like immunoreactivity markedly decreased. The Brattleboro rats resembled untreated rats, except their lack of vasopressin-like immunoreactivity, the marked increase in tyrosine hydroxylase-like immunoreactivity, and smaller increase in galanin- and dynorphin-like immunoreactivity. Addition of colchicine to Brattleboro rats resulted in some distinct further changes in that dynorphin-like immunoreactivity decreased in some neurons and that [Leu]enkephalin-, corticotropin-releasing factor- and peptide histidine-isoleucine-like immunoreactivity increased substantially. Several similarities could be observed between the salt-loaded and Brattleboro rats, with or without colchicine. However, a marked difference in immunoreactive [Leu]enkephalin levels was observed with no difference in dynorphin-like immunoreactivity, and opposite changes in galanin-like immunoreactivity. The results confirm the traditional view that hypothalamic magnocellular neurons in the supraoptic and paraventricular nuclei contain two separate cell populations, characterized by vasopressin and oxytocin, respectively, and that they contain additional messenger molecules in specific patterns. Vasopressin-containing neurons primarily express tyrosine hydroxylase, galanin, dynorphin, [Leu]enkephalin and peptide histidine-isoleucine, and to a minor extent cholecystokinin and thyrotropin-releasing hormone. Oxytocin-containing neurons mainly have cholecystokinin and corticotropin-releasing factor, and to a minor extent galanin, dynorphin, [Leu]enkephalin and thyrotropin-releasing hormone. Furthermore, our results detail individual co-existence situations among these putative messenger molecules. Thus, magnocellular neurons respond in a differential way to various stimuli and they store multiple bioactive substances in specific combinations.
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PMID:Localization of chemical messengers in magnocellular neurons of the hypothalamic supraoptic and paraventricular nuclei: an immunohistochemical study using experimental manipulations. 170 Oct 38

We examined the responses of vasopressin-neurons (VP-neurons) and oxytocin-neurons (OT-neurons) to acute salt-loading in a group of conscious rats (CON, n = 8) and rats under sodium pentobarbital (NEM, 50 mg/kg, i.p., n = 8) or urethane (URE, 1.6 g/kg, i.p. n = 8) anesthesia. Fifteen minutes following the induction of anesthesia, sodium pentobarbital produced an increase in basal plasma osmolality (Posm, 290 +/- 2 to 296 +/- 3 mosm/kg H2O, p less than 0.007) while urethane did not change basal Posm (287 +/- 2 to 289 +/- 2 mosm/kg H2O). Neither anesthetic agent resulted in any significant changes in basal plasma levels of vasopressin-associated neurophysin (VP-RNP) and oxytocin-associated neurophysin (OT-RNP). In response to intravenous infusion of 18% saline, all three groups of rats had similar rises in Posm. The slopes of the relationship between the rise in plasma VP-RNP and the rise in Posm were markedly reduced in both groups of anesthetized animals compared to that observed for conscious animals (CON = 2.54 +/- 0.5; NEM = 1.22 +/- 0.18; URE = 1.17 +/- 0.24 fmol.ml-1.mosm-1.kg H2O-1 p less than 0.0126). The slopes of the relationship between the rise in plasma OT-RNP and the rise in Posm were not significantly (p less than 0.4478) different between the CON group and the NEM group, while the slope for the URE group was significantly (p less than 0.05) smaller than that for the CON group (CON = 10.9 +/- 1.5; NEM = 9.3 +/- 1.5; URE = 6.3 +/- 0.7 fmol.ml-1.mosm-1.kg H2O-1).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of pentobarbital and urethane on release from magnocellular neurons. 174 63

Thoracic shifts of blood stimulate diuresis and natriuresis during spaceflight. The available literature is not conclusive as to whether thoracic afferent neurons are essential for this response. Possibly, an acute elevation in cerebrospinal fluid pressure (CSF-p) activates central compensatory mechanisms. This is because central venous pressure is elevated by thoracic blood shifts and may reduce the pressure gradient for drainage of CSF into the venous sinuses. We tested whether rats with constriction of the venous return at the level of the heart (0.4 mm maximum diameter) had CSF-p different from sham-operated controls. CSF-p in the immediate postoperative period, as well as 1 and 10 days after surgery, were within normal limits and did not differ (p greater than 0.05). Blood collected at the end of the experiment showed no group differences (p greater than 0.05) in the hematocrit, or concentrations of sodium, potassium or vasopressin. Thus, changes in CSF-p, per se, appear to be insufficient to explain the cardiovascular or salt/water balance readjustments observed in spaceflight. It is likely that compensatory systems are highly redundant.
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PMID:Cerebrospinal fluid pressure of conscious rats after venous constriction at the right atrium. 177 18

Plasma renin activity, plasma aldosterone and arginine-vasopressin concentrations were determined in five diarrhoeic and five healthy newborn calves. In animals suffering from diarrhoea these three parameters were 10-15 times higher than those observed in controls. These results suggest that the hormonal systems that control fluid and electrolyte homeostasis are highly stimulated by dehydration and salt depletion induced by faecal losses of water and sodium in calves affected with diarrhoea.
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PMID:Renin-aldosterone system and arginine vasopressin in diarrhoeic calves. 177 95

Hyponatremia is a common electrolyte abnormality in AIDS patients. In this study, hyponatremia was defined as natremia less than 130 mmol/l at two different samplings. Medical records of 160 hospitalized AIDS patients were exhaustively reviewed in search for hyponatremia and, if present, of its etiology. 45 cases of hyponatremia were identified in 43 AIDS patients. Two causes were predominant: hypovolemic hyponatremia, due to water and salt losses (11 cases) and the syndrome of inappropriate antidiuretic hormone secretion (10 cases). These results are consistent with those of the literature and were used to develop a simple diagnosis schedule based on the analysis of limited clinical and biological data: hydration status, serum and urinary osmolality, natriuria and creatininemia.
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PMID:[Hyponatremia in AIDS. Etiology and diagnosis]. 182 21


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