Endogenous opioid mediation of somatostatin inhibition of arginine vasopressin release evoked by insulin-induced hypoglycemia in man

Since suppression of arginine vasopressin (AVP) appears to be a determinant of the diuresis of water immersion (WI) in humans, a further understanding of its responsiveness has important implications for normal physiology, pathophysiology, and space physiology. In recent years, discrepant measurements of AVP in plasma during WI have led to conflicting conclusions. In studies in which the subjects ingested water before or during WI, plasma AVP was reported to be unchanged or even increased. In contrast, plasma AVP was suppressed in studies in which the subjects remained hydropenic. A critical review discloses that water intake before and/or during the experiments introduces several new stimuli for AVP release. Furthermore the lower base-line levels of AVP in hydrated subjects complicate detection of small changes in plasma AVP. Although the mechanisms of AVP suppression during WI are incompletely defined, it appears that not only cardiopulmonary mechanoreceptors but also arterial baroreceptors mediate the response. Additional studies are proposed to delineate further the mechanisms governing AVP release during WI.

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Arginine vasopressin release from human platelets after irreversible aggregation

Clinical Science ◽

10.1042/cs0780113 ◽

1990 ◽

Vol 78 (1) ◽

pp. 113-116 ◽

Cited By ~ 7

Author(s):

Giovanni Anfossi ◽

Elena Mularoni ◽

Mariella Trovati ◽

Paola Massucco ◽

Luigi Mattiello ◽

...

Keyword(s):

Platelet Aggregation ◽

Arginine Vasopressin ◽

Platelet Rich Plasma ◽

Human Platelets ◽

Vasopressin Release ◽

Irreversible Aggregation ◽

Local Release

1. The release of arginine vasopressin from human platelets was investigated in platelet-rich plasma after irreversible aggregation induced by adenosine 5′-pyrophosphate, collagen, sodium arachidonate, thrombin and adrenaline in vitro. 2. Arginine vasopressin levels were significantly higher in the supernatant from stimulated platelet-rich plasma than from unstimulated samples, reaching 3.5 × 10−12 (range 1.6–12.5 × 10−12) mol/l in the absence of an aggregating agent, 8.8 × 10−12 (range 4.2–17.5 × 10−12) mol/l after adenosine 5′-pyrophosphate, 13.7 × 10−12 (2.2–63.2 × 10−12) mol/l after collagen, 7.8 × 10−12 (2.2–14.6 × 10−12) mol/l after sodium arachidonate, 7.8 × 10−12 (2.2–16.3 × 10−12) mol/l after thrombin and 12.2 × 10−12 (4.8–32.1 × 10−12) mol/l after adrenaline. 3. An arginine vasopressin level of 18 × 10−12 mol/l, which can be achieved physiologically, increased the sensitivity of platelets to adenosine 5′-pyrophosphate and collagen in vitro; the same concentration of arginine vasopressin caused a potentiation of the effect of catecholamines on the response of platelets to sodium arachidonate. 4. These results indicate that intraplatelet arginine vasopressin is released during aggregation and suggest that a local release of arginine vasopressin could occur after complete platelet aggregation in vivo.

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Haemodynamic Responses to Acute Blood Loss: New Roles for the Heart, Brain and Endogenous Opioids

Anaesthesia and Intensive Care ◽

10.1177/0310057x8901700312 ◽

1989 ◽

Vol 17 (3) ◽

pp. 312-319 ◽

Cited By ~ 5

Author(s):

A. F. Van Leeuwen ◽

R. G. Evans ◽

J. Ludbrook

Keyword(s):

Blood Pressure ◽

Blood Loss ◽

Peripheral Resistance ◽

Endogenous Opioids ◽

Acute Blood Loss ◽

Endogenous Opioid ◽

Vasopressin Release ◽

Arterial Blood ◽

Blood Pressure Fall ◽

Human Volunteers

Information has come forward recently from several sources which provides new insights into the mechanisms that underlie the haemodynamic responses to acute blood loss. In unanaesthetised animals and human volunteers there are two distinct phases to these responses. At first, the engagement of baroreflexes results in a progressive rise in sympathetic vasoconstrictor drive and peripheral resistance, and the maintenance of arterial blood pressure at a near-normal level. When about one-third of blood volume has been lost, reflex sympathetic drive is switched off, and peripheral resistance and blood pressure fall abruptly to low levels despite a burst of vasopressin release. Research in conscious animals has now shown that the onset of this decompensatory phase is triggered by a signal from the heart, which activates an endogenous opioid mechanism in the brain. Activation of this mechanism can be prevented by administering a selective δ-receptor antagonist, or selective μ-receptor agonists (including alfentanil). It has not yet been established that this endogenous opioid mechanism is responsible for the decompensatory phase of acute blood loss in man, nor that it can be prevented or reversed by selective opioid agonists or antagonists.

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Lipopolysaccharide increases arginine-vasopressin release from rat suprachiasmatic nucleus slice cultures

Neuroscience Letters ◽

10.1016/s0304-3940(00)01199-x ◽

2000 ◽

Vol 288 (3) ◽

pp. 228-230 ◽

Cited By ~ 18

Author(s):

Felice Nava ◽

Giovanna Carta ◽

Laurence W Haynes

Keyword(s):

Suprachiasmatic Nucleus ◽

Arginine Vasopressin ◽

Vasopressin Release

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Centrally administered galanin inhibits osmotically stimulated arginine vasopressin release in conscious rats

Neuroscience Letters ◽

10.1016/0304-3940(91)90271-t ◽

1991 ◽

Vol 128 (2) ◽

pp. 245-248 ◽

Cited By ~ 24

Author(s):

Kunikazu Kondo ◽

Takashi Murase ◽

Kazuo Otake ◽

Masafumi Ito ◽

Yutaka Oiso

Keyword(s):

Arginine Vasopressin ◽

Vasopressin Release ◽

Conscious Rats

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Effects of high altitude and water deprivation on arginine vasopressin release in men

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00332.2003 ◽

2004 ◽

Vol 286 (1) ◽

pp. E20-E24 ◽

Cited By ~ 17

Author(s):

C. M. Maresh ◽

W. J. Kraemer ◽

D. A. Judelson ◽

J. L. VanHeest ◽

L. Trad ◽

...

Keyword(s):

High Altitude ◽

Sea Level ◽

Arginine Vasopressin ◽

Water Deprivation ◽

Urine Volume ◽

Plasma Osmolality ◽

Vasopressin Release ◽

Altitude Exposure ◽

Blood Pressures ◽

Healthy Males

High-altitude exposure changes the distribution of body water and electrolytes. Arginine vasopressin (AVP) may influence these alterations. The purpose of this study was to examine the effect of a 24-h water deprivation trial (WDT) on AVP release after differing altitude exposures. Seven healthy males (age 22 ± 1 yr, height 176 ± 2 cm, mass 75.3 ± 1.8 kg) completed three WDTs: at sea level (SL), after acute altitude exposure (2 days) to 4,300 m (AA), and after prolonged altitude exposure (20 days) to 4,300 m (PA). Body mass, standing and supine blood pressures, plasma osmolality (Posm), and plasma AVP (PAVP) were measured at 0, 12, 16, and 24 h of each WDT. Urine volume was measured at each void throughout testing. Baseline Posm increased from SL to altitude (SL 291.7 ± 0.8 mosmol/kgH2O, AA 299.6 ± 2.2 mosmol/kgH2O, PA 302.3 ± 1.5 mosmol/kgH2O, P < 0.05); however, baseline PAVP measurements were similar. Despite similar Posm values, the maximal PAVP response during the WDT (at 16 h) was greater at altitude than at SL (SL 1.7 ± 0.5 pg/ml, AA 6.4 ± 0.7 pg/ml, PA 8.7 ± 0.9 pg/ml, P < 0.05). In conclusion, hypoxia appeared to alter AVP regulation by raising the osmotic threshold and increasing AVP responsiveness above that threshold.

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Atrial natriuretic peptide inhibits osmolality-induced arginine vasopressin release in man

Clinical Science ◽

10.1042/cs0750035 ◽

1988 ◽

Vol 75 (1) ◽

pp. 35-39 ◽

Cited By ~ 15

Author(s):

M. J. Allen ◽

V. T. Y. Ang ◽

E. D. Bennett ◽

J. S. Jenkins

Keyword(s):

Atrial Natriuretic Peptide ◽

Natriuretic Peptide ◽

Arginine Vasopressin ◽

Plasma Osmolality ◽

Random Order ◽

Vasopressin Release ◽

Plasma Arginine ◽

Placebo Infusion ◽

Atrial Natriuretic

1. Eight normal volunteers were infused with 5% saline (5 g of NaCl/100 ml) at a rate of 0.06 ml min−1 kg−1 for 120 min to increase plasma osmolality and plasma arginine vasopressin. Human atrial natriuretic peptide (α-hANP; 100 μg) or placebo was given in random order in a double-bind cross-over design for the last 20 min of the saline infusion. 2. Compared with the placebo infusion, atrial natriuretic peptide (ANP) produced a 43% greater sodium excretion and a 34% greater urinary volume in the subsequent hour. 3. Mean plasma immunoreactive ANP did not increase in response to changes in osmolality and rose to a peak of 118 pg/ml during the α-hANP infusion. α-hANP produced significant suppression of mean plasma arginine vasopressin over the 60 min after the infusions. 4. We conclude that ANP is not released in response to increased osmolality in vivo, and that it inhibits osmolality-induced arginine vasopressin release in man.

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