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)

Arginine vasopressin, a potent vasoconstrictor and regulator of body water, is frequently increased in the plasma of patients with congestive heart failure. Other neurohumoral control networks, such as the sympathetic nervous system and the renin-angiotensin system, also demonstrate increased activity in congestive heart failure, but fail to respond normally to physiologic stress, such as orthostatic tilt. To assess the response of plasma vasopressin to orthostasis in heart failure, vasopressin was measured before and at 10 and 45 minutes during passive upright tilt in 15 patients with congestive heart failure and their response was compared with that in 9 normal control subjects. Arginine vasopressin was measured by radioimmunoassay. In the normal subjects, plasma arginine vasopressin was 5.3 +/- 2.3 pg/ml at control, was unchanged at 10 minutes, but significantly increased to 7.0 +/- 2.5 pg/ml at 45 minutes (p less than 0.05). In contrast, patients with congestive heart failure showed no significant changes in arginine vasopressin levels from the control levels of 11.6 +/- 5.5 pg/ml. Both plasma norepinephrine and renin activity increased in the normal subjects, but failed to increase from higher baselines in patients with congestive heart failure. Thus, plasma arginine vasopressin, like plasma norepinephrine and renin activity, does not increase in response to upright tilt in patients with congestive heart failure. The explanation is not evident but could involve either abnormalities in reflex control of plasma vasopressin in congestive heart failure or in clearance of the hormone during orthostasis.
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PMID:Impaired response of plasma vasopressin to orthostatic stress in patients with congestive heart failure. 635 40

Arginine vasopressin (AVP) and angiotensin II (ANG II) reduce the glomerular filtration rate and ultrafiltration coefficient. Vasodilatory prostaglandins (PG) antagonize these effects. AVP and ANG II also cause mesangial cell contraction. Therefore, possible PG stimulation by these peptides and two vasopressin analogues was studied in cultured rat glomerular mesangial cells. The effect of altered calcium availability on PG production was also studied. Glomeruli from 75-100-g Sprague-Dawley rats were cultured in supplemented nutrient media for 28 d and experiments were performed on the first passage. Mesangial cell morphology was confirmed by electron microscopy. Cells produced PGE2 much greater than PGF2 alpha greater than 6-keto-PGF1 alpha greater than thromboxane B2 when incubated with the divalent cation ionophore, A23187, or arachidonic acid (C20:4). ANG II and AVP selectively stimulated PGE2 at threshold concentrations of 10 nM ANG II and 100 pM of AVP. The effects of the antidiuretic analogue 1-desamino-8-D-arginine vasopressin (dDAVP) and the antipressor analogue [1-(beta-mercapto-beta beta-cyclopentamethylene propionic acid)-4-valine, 8-D-arginine]-vasopressin (d[CH2]5VDAVP), were studied. Neither compound stimulated PGE2 and preincubation with d(CH2)5VDAVP abolished, and dDAVP blunted, AVP-enhanced PGE2 production. Incubation in verapamil, nifedipine, or zero calcium media blocked peptide-stimulated PGE2 production. Increasing extracellular calcium or adding A23187 increased PGE2 synthesis. Selective stimulation of PGE2 by ANG II or AVP in mesangial cells suggests a hormone-sensitive phospholipase and a coupled cyclooxygenase capable of synthesizing only PGE2. Since neither vasopressin analogue stimulated PGE2, but both blocked AVP-enhanced PGE2 production, we conclude that these cells respond to the pressor activity of AVP. This is a calcium-dependent process. Selective stimulation of PGE2 by ANG II and AVP may modulate their contractile effects on the glomerulus.
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PMID:Prostaglandin synthesis by rat glomerular mesangial cells in culture. Effects of angiotensin II and arginine vasopressin. 640 23

Arginine vasopressin (AVP) was released in vitro in a pulsatile pattern from the hypothalamo-neurohypophyseal system (HNS) and from the hypothalamus during continuous hyperosmotic stimuli with NaCl or fructose. No significant difference was found in the AVP pulse frequency between the two kinds of hyperosmotic agents. AVP was released from the HNS in a dose-related manner under NaCl stimulation. When the neural lobe was stimulated with NaCl or fructose, a clear AVP pulse pattern was not apparent. Urea failed to evoke a significant AVP release from the neural lobe or HNS. A stepwise increase in NaCl stimulation from 5 to 25 mEq induced a AVP response from the HNS and hypothalamus similar to that under constant stimulation at 25 mEq NaCl. This phenomenon was also found with fructose or sucrose. These results suggest that AVP release from the HNS during continuous osmotic stimulation has a pulsatile pattern regardless of the hyperosmotic substance or osmotic pressure. This AVP release accurately reflects the physiological function of the hypothalamus without modulation in the neural lobe. These results also suggest that the total amount of AVP was related to the osmotic pressure or the osmotic substance but that the frequency of the pulse release was not, moreover, that the AVP release depends not only on the absolute osmotic pressure, but also on the changing rate of osmotic pressure.
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PMID:Pulsatile arginine vasopressin release from the rat hypothalamo neurohypophyseal system during osmotic stimulation. 645 10

Arginine vasopressin (AVP), lysine vasopressin (LVP) and [des-9-glycinamide]LVP (DGLVP), administered systemically, delayed the disappearance of functional tolerance to the motor-incoordinating effect of ethanol in mice. This result is consistent with previous findings that AVP and related neuropeptides maintain tolerance to the sedative-hypnotic and hypothermic effects of ethanol, and suggests that the peptides modulate the rate of disappearance of tolerance per se, rather than simply influencing the tests used to evaluate tolerance. However, both the duration of tolerance to the incoordinating effect of ethanol, and the duration of peptide maintenance of this tolerance, were less than those observed for tolerance to the hypnotic and hypothermic effects of ethanol. Tolerance to various effects of ethanol clearly can develop and dissipate at different rates, and our results suggest that the characteristics of the maintenance of ethanol tolerance by neurohypophyseal peptides are influenced, to some extent, by the neural systems which mediate the expression of the functional tolerance which is being investigated.
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PMID:Neurohypophyseal peptides maintain tolerance to the incoordinating effects of ethanol. 650 51

Although it is well established that chronic treatment with antidiuretic hormone increases renal prostaglandin (PG) excretion, the effects of short-term infusions are controversial. Therefore, in the present study the effect of acute administration of arginine vasopressin on urinary PG excretion was investigated in conscious Brattleboro rats and in water-diuresing Long-Evans rats. Water balance was kept constant during arginine vasopressin infusion. Arginine vasopressin caused a significant, dose-related and reversible increase in urinary PG excretion within 20 min in both models. Similar results were obtained during the infusion of 1-deamino-8-D-arginine vasopressin in the Brattleboro rat. Normalization of the hydropenia of Brattleboro rats by infusion of large amounts of hypotonic fluid failed to elevate urinary PG excretion. These results give no support to the hypothesis that the acute enhancement of urinary PG excretion by vasopressin is mediated through either vasoconstriction or volume retention or induction of cyclooxygenase, but rather they indicate that antidiuretic hormone can increase renal PG synthesis through a more direct mechanism in vivo.
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PMID:Acute effects of antidiuretic hormone on urinary prostaglandin excretion. 657 22

Rat tail arteries were incubated overnight in potassium (K)-free physiological saline solution (PSS) at 10 degrees C, then returned to normal aerated PSS at 37 degrees C for a 3-hour recovery period followed by standard chemical analysis. Cell sodium (Na) was measured following replacement of extracellular Na by lithium (Li) at 3 degrees C. The addition of aldosterone at 10(-7) M reduced free cell Na by about 3 mmol/kg dry weight (about 20%). Arginine vasopressin also lowered cell Na to the same degree. The minimal effective dose was about 25 pM (25 pg/ml, 0.01 mU/ml), and the maximal dose was about 250 pM. No effect was seen with higher doses (greater than 1.5 nM or 0.5 mU/ml). Tissues incubated in media containing 10(-7) M aldosterone showed an exaggerated response to vasopressin evidenced by a near doubling of the maximum fall in cell Na produced by a tenfold smaller dose (25 pM). No significant change in cell K was observed while cell water tended to increase with lower doses. Angiotensin produced a similar reduction of cell Na at the same dose levels as vasopressin and was similarly additive with aldosterone. We suggest that these hormones enhance the transport of Na from luminal to basal sides of polarized cells and from cells to environment in symmetrical cells.
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PMID:Additive effects of aldosterone with vasopressin or angiotensin. 672 64

The object of this study was to determine the importance of vasoconstrictor activity in the suppression of renin secretion by vasopressin. Arginine vasopressin (AVP) (0.05 and 0.1 ng/kg/min) and a nonpressor analogue of vasopressin, 1-deamino-[4-threonine, 8-D-arginine]-vasopressin (dTDAVP) (0.01 and 0.05 ng/kg/min), were infused intravenously in anesthetized hypophysectomized dogs. Neither dTDAVP nor AVP influenced arterial pressure or heart rate but both suppressed plasma renin activity. Infusion of dTDAVP at 0.01 and 0.05 ng/kg/min suppressed plasma renin activity to 86 +/- 4% (p less than 0.05) and 63 +/- 6% (p less than 0.01) of the control values respectively. Infusion of AVP at 0.05 and 0.1 ng/kg/min suppressed plasma renin activity to 60 +/- 8% (p less than 0.01) and 59 +/- 12% (p less than 0.05) of the control values respectively. dTDAVP and AVP both produced significant increases in sodium excretion. These data demonstrate that vasoconstrictor activity is not required for the effects of vasopressin on renin secretion and sodium excretion.
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PMID:Effects of a nonpressor analogue of vasopressin on plasma renin activity and salt and water excretion in water-loaded, anesthetized dogs. 675 35

1. The corticotrophin releasing activity of hypothalamic extracts from rats congenitally lacking vasopressin (Brattleboro strain) has been studied in the presence and absence of arginine vasopressin and its antiserum. 2. Hypothalamic extracts from Brattleboro rats stimulated the production of corticotrophin by pituitary segments in vitro but both their potency and the slopes of their dose-response lines were significantly less than those of controls. Arginine vasopressin also stimulated pituitary-adrenocorticotrophic activity in vitro but only in concentrations considerably greater than those present in hypothalamic extracts from normal rats. 3. In low, physiological concentrations arginine vasopressin did not affect the corticotrophin releasing activity of hypothalamic extracts from controls but potentiated markedly the activity of extracts from Brattleboro rats and rendered the slopes of their dose-response lines parallel with those of the controls. 4. The antiserum to arginine vasopressin did not affect the corticotrophin releasing activity of Brattleboro extracts but reduced the activity of control extracts and rendered the slopes of their dose-response lines parallel with those of Brattleboro extracts. 5. The results suggest that vasopressin acts synergistically with the corticotrophin releasing factor and is essential for the full expression of pituitary-adrenocorticotrophic activity.
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PMID:The influence of vasopressin on hypothalamic corticotrophin releasing activity in rats with inherited diabetes insipidus. 697 27

It is known that vasopressin decreases PRA and heart rate and increases blood pressure and plasma corticosteroid concentration. The purpose of this study was to determine the plasma concentration of vasopressin required to produce these effects. Arginine vasopressin was administered iv to five normal conscious dogs as priming injections of 0.1, 0.5, 1.0, 2.5, 5.0, and 10.0 ng/kg, followed by infusions of 0.01, 0.05, 0.1, 0.25, 0.5, and 1.0 ng/kg x min, respectively, for 30 min. These doses produced increases in the plasma vasopressin concentration (+/- SE) of 1.0 +/- 0.8, 2.1 +/- 4.3, 4.3 +/- 1.8, 11.4 +/- 1.0, 19.7 +/- 6.4, and 30.8 +/- 7.8 pg/ml, respectively, from a basal level of 2.7 +/- 0.2 pg/ml. An increase in the plasma vasopressin concentration of 2.1 +/- 0.3 pg/ml suppressed PRA by 19 +/- 5% (P < 0.02); increases of 4.2 +/- 1.8 pg/ml or more suppressed PRA by 34 +/- 12% (P < 0.005). Only the highest dose of vasopressin produced a significant pressor effect (9 +/- 3 mm Hg; P < 0.05) or lowered the heart rate (18 +/- 4 beats/min; P < 0.005). An increase in plasma vasopressin concentration of 19.7 +/- 6.4 pg/ml was required to increase the plasma corticosteroid concentration (1.2 +/- 0.2 to 2.2 +/- 0.4 microgram/dl; P < 0.01); the largest dose of vasopressin increased the plasma corticosteroid concentration from 1.5 +/- 0.1 to 2.4 +/- 0.6 microgram/dl (P < 0.02). Twenty-four-hour water deprivation in the same dogs increased the plasma vasopressin concentration from 2.5 +/- 0.2 to 7.4 +/- 0.6 pg/ml (P < 0.01). Nonhypotensive hemorrhage in another group of dogs increased the plasma vasopressin concentration from 2.5 +/- 0.2 to 47.4 +/- 16.8 pg/ml (P < 0.05). These data indicate that elevations in the plasma vasopressin concentration within the range observed during 24 h of water deprivation and nonhypotensive hemorrhage produced significant decreases in renin secretion and heart rate and elevations in blood pressure and corticosteroid secretion.
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PMID:Effects of increases in plasma vasopressin concentration on plasma renin activity, blood pressure, heart rate, and plasma corticosteroid concentration in conscious dogs. 700 May 4

Arginine vasopressin, the antidiuretic hormone in man, in low concentrations increases reabsorption of water in the collecting ducts of the kidney, producing a concentrated urine. It is also a potent vasoconstrictor because of its direct effect on arteriolar smooth muscle, particularly the splanchnic, renal, and coronary vascular beds. This appears to be a dose-dependent response. In very high concentrations it is capable of producing a diuresis with increased urinary sodium excretion. The preponderance of evidence today has failed to show any significant increase in antidiuretic hormone levels with anesthesia alone, provided significant hemodynamic changes do not occur. It seems unlikely, then, that the inhalation anesthetics or high-dose narcotic anesthesia are a direct stimulus to ADH release. If a decrease in urine flow does occur, it is more likely caused by either the renal hemodynamic effects of the anesthetic or a secondary release of ADH. Surgical stimulation is capable of significantly increasing ADH levels. This apparently is a stress response that can be attenuated by the depth of anesthesia. Such a response to operation may produce ADH levels that can indeed decrease urinary flow, but more importantly may succeed in achieving levels that can exert a significant vasopressor effect. In unusual circumstances, vasopressin levels can occur that are capable of producing a diuresis and increased urine sodium excretion.
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PMID:The effects of anesthesia on antidiuretic hormone. 701 72


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