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)

Plasma levels of immunoreactive alpha human atrial natriuretic peptide (IR-ANP) were measured in nine patients with chronic renal failure before and after removal of 1.3-3.7 litres of fluid by ultrafiltration and again during volume repletion with intravenous sodium chloride solution (150 mmol/l: saline). Baseline levels of IR-ANP were elevated but fell by 22% during ultrafiltration. Saline infusion induced a rapid and steep rise in IR-ANP levels which were 150% of baseline while body weight was still 2% below baseline. Changes in plasma renin, angiotensin II, aldosterone and vasopressin during the study were slight compared with the change in IR-ANP, but noradrenaline levels rose threefold during ultrafiltration. There was a significant positive relationship between arterial pressure and IR-ANP levels before and after ultrafiltration. These results lend support to the suggestion that atrial peptides are of physiological importance, especially in states of chronic fluid overload such as chronic renal failure.
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PMID:Exaggerated responsiveness of immunoreactive atrial natriuretic peptide to saline infusion in chronic renal failure. 294 53

The effects of the opioid antagonist naloxone on the vasopressin (AVP) and oxytocin (OT) responses to nicotine were studied in male non-smokers (21-30 years old). Either saline (n = 6) or naloxone (4 mg bolus + 6 mg/h, n = 6) was infused i.v. during the study. After 60 min infusion the subjects smoked one high-nicotine content cigarette. Naloxone infusion for 60 min did not alter basal plasma AVP or OT levels. Smoking led to a significant rise in plasma vasopressin in both saline and naloxone-infused subjects (P less than 0.05). There was no significant difference in the plasma AVP response to smoking between the two groups. Saline-infused subjects did not show any change in plasma OT in response to smoking. Naloxone infusion was associated with a significant rise in OT from 1.3 +/- 0.1 pmol/l to 4.3 +/- 2.4 pmol/l 5 min after smoking (P less than 0.05). We conclude that there is endogenous opioid-mediated inhibition of OT which prevents its release when AVP is secreted in response to nicotine in man.
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PMID:Endogenous opioids inhibit oxytocin release during nicotine-stimulated secretion of vasopressin in man. 321 43

Regeneration and functional recovery of the hypothalamoneurohypophysial system (HNS) in neurohypophysectomized rats treated with either saline or vasopressin (VP) were analyzed utilizing specific immunohistochemical and physiological measures. Neural lobe ablation combined with VP administration precipitated a profound diabetes insipidus (following cessation of VP delivery) that persisted for the duration of the experiment. Diabetes insipidus was correlated with a drastic reduction in the number of VP-positive neurons in magnocellular hypothalamic nuclei. In contrast, large numbers of oxytocin (OT)-positive neurons survived neurohypophysectomy in VP-treated neurohypophysectomized rats; OT neurons accounted for the vast majority of magnocellular profiles observed in Nissl-counterstained sections. VP-immunoreactive fibers could be observed in limited quantities in the external lamina of the median eminence of VP-treated neurohypophysectomized rats, with little staining evident in the internal lamina. Saline-treated neurohypophysectomized rats exhibited the recovery of antidiuretic function characteristically seen following this lesion, with evidence of survival of considerable numbers of VP and OT neurons and median eminence hypertrophy. Both the internal and external laminae of the median eminence were densely innervated by large-caliber VP and OT fibers. Sham-operated animals receiving VP treatment did not show any long-term deficit in water metabolism, changes in the complement of VP or OT perikarya in hypothalamus, or changes in the innervation of the median eminence. Results indicate that VP treatment following neurohypophysectomy results in extensive retrograde degeneration of magnocellular VP neurons without affecting the survival of OT cells.
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PMID:Selective cell death of magnocellular vasopressin neurons in neurohypophysectomized rats following chronic administration of vasopressin. 330 29

Pressor responses to arginine-vasopressin (AVP) and norepinephrine (NE) were studied in deoxycorticosterone (DOC)-salt hypertensive and prehypertensive rats. DOC-salt rats received weekly subcutaneous injection of DOC acetate (30 mg/kg) and given 1% saline for drinking. Salt and control rats received injections of sesame oil and given 1% saline or tap water, respectively. On the 5th day (prehypertensive stage) and at 6th week (hypertensive stage) after treatment had started, pressor responses were studied by measuring changes in mean arterial pressure recorded from the iliac artery in response to i.v. injections of AVP or NE under urethane anesthesia. Pressor response to AVP was enhanced both in DOC-salt hypertensive and prehypertensive rats compared with that in salt and control rats. Pressor response to NE tended to be enhanced in DOC-salt hypertensive rats, however, the enhancement was not observed in the rats in prehypertensive stage. Enhanced pressor response to AVP in DOC-salt prehypertensive rats was not due to the structural change of vascular beds, because peripheral resistance in isolated hindlimb preparations was similar in the three groups. Thus, pressor response to AVP was enhanced even in the prehypertensive stage in DOC-salt rats and the enhancement might be involved in the pathogenesis of hypertension in DOC-salt rats.
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PMID:Pressor response to vasopressin and norepinephrine in DOC-salt hypertensive and prehypertensive rats. 338 Dec 22

In the pithed Wistar rats Captopril (2 mg/kg) decreased the mean arterial pressure (MAP) 21%. Further injection of a specific antagonist decreased the vasoconstrictor action of vasopressin (aAVP, 10 micrograms/kg) an additional 6%. Reversal in the order of drug administration did not change these percentages. The osmotic stimulus evoked by the infusion of hypertonic saline (ClNa 9%, 0.018 ml/min, 2 hr) significantly increased MAP, this increase being almost totally reversed by the aAVP (10 micrograms/kg). These findings suggest a greater role of the renin-angiotensin system than of the vasopressin (AVP) in the maintenance of MAP in the pithed rat; AVP, moreover, can be released by means of an osmotic stimulus.
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PMID:Blood pressure control in pithed rat. 353 Aug 77

Heterozygous Brattleboro (HZ) rats exhibit a partial genetic deficiency in hypothalamic vasopressin (VP) production. The effects of this abnormality of HZ rats on the capacities of VP-neurons and oxytocin (OT)-neurons to respond to an acute salt-load were examined. Acute salt-loading was induced by intravenous infusion of 18% saline in conscious, chronically catheterized animals and the activities of VP-neurons and OT-neurons were interpreted from plasma concentrations of VP-associated neurophysin, [VP-RNP] and OT-associated neurophysin, [OT-RNP] at different time periods throughout the infusion. Plasma sodium concentration ([Na+]), plasma osmolality (Posm) and mean arterial pressure (MAP) were also monitored. Salt-loading produced significant rises in [VP-RNP] and [OT-RNP]. These rises were accompanied by increases in plasma [Na+], Posm and MAP. Releases of OT-RNP were approximately four times greater than those of VP-RNP. The responsiveness of VP-neurons to increases in Posm in the HZ rat was approximately one-half of that observed for the Long-Evans (LE) rat. Furthermore, the responsiveness of OT-neurons in these animals was approximately one-half of that for LE rats and one-third of that for homozygous Brattleboro (DI) rats. The changes in MAP during salt-loading do not appear to be different for HZ and LE rats. Hence, while VP may be involved in the rise in blood pressure during infusion of hypertonic saline, there is not a direct correlation between plasma levels of VP-RNP (and presumably VP) and rises in blood pressure.
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PMID:Reduced responsiveness to acute salt-loading of vasopressin-neurons and oxytocin-neurons in the heterozygous Brattleboro rat. 357 2

Although the steps involved in biosynthesis and secretion of the neuropeptide vasopressin (AVP) have been extensively studied, the factors which regulate AVP gene expression remain unknown. Therefore, we sought to determine the dynamics of AVP mRNA accumulation in response to a strong stimulus for AVP release, i.e. during salt imbibition and the ensuing period of rehydration. AVP mRNA levels were determined in terms of absolute amounts by a novel quantitative densitometric hybridization assay, using in vitro synthesized sense-strand RNA as a quantitative standard and complementary anti-sense RNA as a specific probe. The template used for RNA transcription consisted of a 196-base pair genomic DNA fragment corresponding to exon C of the rat AVP gene. Determination of basal hypothalamic AVP mRNA levels yielded 12.5 +/- 2.7 fmol/hypothalamus. Salt imbibition, which induced a 6% rise in blood osmolality and an 82% loss of pituitary AVP, resulted in a 3-fold increase of AVP mRNA to 35 +/- 5 fmol/hypothalamus. Following rehydration, plasma osmolality returned to control levels by day 2, pituitary AVP by day 6, and hypothalamic AVP by day 14. By contrast, AVP mRNA levels remained significantly elevated throughout the 30-day rehydration period. Furthermore, pituitary AVP reached a level of 177% of control by day 14 of rehydration. These data show that osmotic stimulation results in a long-lasting elevation of hypothalamic AVP mRNA; during rehydration, these elevated mRNA levels direct AVP biosynthesis at a rate which surpasses secretory demands; AVP mRNA accumulation does not appear to be directly regulated by either pituitary or hypothalamic AVP. Therefore, either an unusually long half-life of greater than or equal to 7 days must be assumed for AVP mRNA or, alternatively, a continued stimulation of AVP gene transcription must occur, even in the absence of a secretory stimulus and following complete repletion of cellular AVP stores.
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PMID:Regulation of vasopressin gene expression in rat hypothalamic neurons. Response to osmotic stimulation. 375 44

We studied the effects of chronic replacement with arginine vasopressin (AVP) or 1-desamino-D-arginine vasopressin (DDAVP), as well as acute replacement with AVP or DDAVP, on the responsiveness of oxytocin (OT) neurons as indexed by plasma oxytocin-associated neurophysin concentration [( OT-RNP]) during acute salt loading in conscious, chronically catheterized homozygous Brattleboro (DI) rats. Salt loading was carried out on days 5 and 12 of AVP (3,000 ng/day) or DDAVP (50 ng/day) treatment or 60 min after intraperitoneal injection of 1 microgram AVP or 25 ng DDAVP. All vasopressin treatments did not significantly alter the basal [OT-RNP]. In response to infusion of 18% saline, there were corresponding significant increases in plasma osmolality (Posmol) and [OT-RNP] in all animals. The increases in [OT-RNP] in vasopressin-treated DI rats were markedly reduced compared with those observed earlier for untreated DI animals despite similar rises in Posmol. The slopes of the relationship between delta [OT-RNP] and delta Posmol were 9.0 and 9.8 fmol X ml-1 X mosmol-1 X kg for chronically AVP-treated DI rats, 8.9, and 8.8 fmol X ml-1 X mosmol-1 X kg for chronically DDAVP-treated DI animals, 10.7 fmol X ml-1 X mosmol-1 X kg for acutely AVP-treated DI rats, and 8.3 fmol X ml-1 X mosmol-1 X kg for acutely DDAVP-treated animals compared with that of 34.9 fmol X ml-1 X mosmol-1 X kg for untreated DI rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Exogenous vasopressin modulates activity of oxytocin neurons in homozygous Brattleboro rats. 377 64

As a model to study effects of chronic, excessive salt loading on circulation, Pekin ducks were adapted to 2% saline solution as their sole water supply, while fresh-water-adapted animals were used as controls. Due to the development of salt-eliminating glands, salt-adapted ducks are able to cope indefinitely with this salt stress which means a daily ingestion of 5-6 g NaCl per kg body weight per day, associated with a chronic elevation of plasma osmolality and plasma sodium by 5-8% above normal and an up to 3-fold increase of antidiuretic hormone concentration in comparison to animals maintained on fresh water. Salt loading for up to 14 months did neither increase arterial mean, nor diastolic, nor pulse pressure. On the contrary, arterial mean and diastolic pressure were slightly lower in the salt-adapted than in the fresh-water-adapted animals, while pulse pressure and heart rate did not differ. Circulatory adaptation to removal and reinfusion of 10% of the estimated blood volume was identical in salt-water and fresh-water-adapted ducks. It is concluded that even excessive chronic salt loading resulting in chronic hyperosmolality with high plasma levels of sodium and antidiuretic hormone does not alter hemodynamic adaptation, provided that efficient compensating mechanisms are at the animal's disposal.
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PMID:Blood pressure and arginine vasotocin in normonatremic and hypernatremic ducks. 400 22

The renal concentrating ability (RCA) was studied in 30 obese subjects before and after modified fasting (MF) and T3 supplementation, and during hypocaloric-carbohydrate refeeding. We also studied the effect of sodium supplementation on the RCA during MF. Modified fasting induced a low T3-high rT3 state ("sick euthyroid"). During T3-supplementation plasma T3 levels increased but were in the normal range for normal weight controls. Plasma sodium, potassium, and calcium remained within the normal range during all study periods. After MF (14 days) the mean maximal urinary osmolality was significantly lower compared to prefast values both after dehydration alone (706 +/- 12 mosm/kg H2O v 975 +/- 14, P less than 0.001) and after dehydration plus sc vasopressin administration (676 +/- 19 v 899 +/- 17, P less than 0.001). After 14 days MF followed by 14 days MF + T3-supplementation plasma urea, urinary urea excretion, and the creatinine clearance were significantly greater than after MF alone as was the RCA (764 +/- 15 v 652 +/- 25, P less than 0.002). Sodium chloride supplementation increased RCA (P less than 0.02) but no additive effect of T3 and sodium chloride supplementation was observed. Severe dietary salt restriction induced a significant decline in RCA (P less than 0.005). Refeeding with carbohydrate increased plasma T3 from 79.9 +/- 7.7 to 97 +/- 7.5 ng/100 mL (NS) and decreased plasma rT3 from 0.33 +/- 0.02 to 0.27 +/- 0.02 ng/mL, (P less than 0.02); no significant change in RCA was observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal concentrating ability in obesity. Effect of modified fasting and the supplementation of T3, sodium chloride and carbohydrate. 405 11


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