Effects of water immersion on arginine vasopressin release in humans

1988 ◽  
Vol 64 (1) ◽  
pp. 1-10 ◽  
Author(s):  
P. Norsk ◽  
M. Epstein
Keyword(s):  
Water Intake ◽  
Arginine Vasopressin ◽  
Critical Review ◽  
Water Immersion ◽  
Base Line ◽  
Vasopressin Release ◽  
Arterial Baroreceptors ◽  
Lower Base

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.

Vasopressin release in sheep following various degrees of rehydration

1987 ◽  
Vol 253 (4) ◽  
pp. R640-R645 ◽  
Author(s):  
J. R. Blair-West ◽  
A. P. Gibson ◽  
S. J. Sheather ◽  
R. L. Woods ◽  
A. H. Brook
Keyword(s):  
Water Intake ◽  
Arginine Vasopressin ◽  
Total Protein ◽  
Plasma Osmolality ◽  
Constant Infusion ◽  
Vasopressin Release ◽  
Extravascular Space ◽  
Rapid Fall ◽  
Disappearance Curve ◽  
Plasma Arginine

Restriction of the water intake of sheep to 0.5 1/day for 7-9 days increases plasma arginine vasopressin (pAVP), and voluntary rehydration causes a rapid fall in pAVP with no change in plasma osmolality. The extent of that inhibition of AVP release was assessed by comparing the decline of pAVP after drinking with pAVP disappearance curves obtained in the same sheep after stopping a constant infusion of AVP at 0.5 micrograms/h, which increased pAVP to the dehydration level. The fall in pAVP after drinking was almost identical with the disappearance curve showing that AVP release was almost completely inhibited during the 2-3 min taken for the sheep to drink 3-5 liters to satiate themselves. The response seemed, therefore, to be cued before the intake reached the satiating volume. When dehydrated sheep drank only 0.5 or 1.0 liter, in 30 s or less, pAVP again fell rapidly but only to a minimum approximately 15 min after drinking. The pAVP was unaltered in dehydrated sheep presented with water but denied access to it. Thus satiation was not necessary for rapid inhibition of AVP release after drinking, but satiation was necessary for this inhibition to be maintained. The initial inhibition was associated with falls in hematocrit and plasma total protein but not plasma osmolality. This isosmolar dilution occurred even in sheep that saw but were denied access to the water and suggests a shift of fluid from the extravascular space.

Arginine vasopressin release from human platelets after irreversible aggregation

1990 ◽  
Vol 78 (1) ◽  
pp. 113-116 ◽  
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.

Fetal recirculation of amniotic fluid arginine vasopressin

1986 ◽  
Vol 250 (3) ◽  
pp. E253-E258
Author(s):  
M. G. Ervin ◽  
M. G. Ross ◽  
R. D. Leake ◽  
D. A. Fisher
Keyword(s):  
Amniotic Fluid ◽  
Arginine Vasopressin ◽  
Urine Volume ◽  
Fetal Lung ◽  
Biologically Active ◽  
Base Line ◽  
Lung Fluid ◽  
Fetal Plasma ◽  
Urine Production ◽  
Fetal Urine

Amniotic fluid volume reflects a balance between fetal lung fluid and fetal urine production and fluid reabsorption via fetal swallowing. Arginine vasopressin (AVP) infusion decreases both fetal lung fluid and urine production and increases amniotic fluid osmolality and AVP concentration. In the present study we assessed the effect of amniotic fluid AVP injection on plasma AVP (n = 6) and renal function (n = 4) in chronically catheterized fetal lambs (X gestation = 130 days). Thirty minutes after addition of 25 micrograms of synthetic AVP into the amniotic cavity, mean +/- SE fetal plasma AVP increased from a base line of 2.7 +/- 0.2 to 14.6 +/- 3.4 pg/ml (P less than 0.01). One hundred and twenty minutes after injection, plasma AVP had increased to 26.9 +/- 5.7 pg/ml. Fetal urine volume did not change (0.78 +/- 0.01 ml/min) but significant increases in urine osmolality (169 +/- 19 to 315 +/- 25 mosm) and urine sodium (64 +/- 11 to 125 +/- 11 mueq/ml) were observed 120 min after AVP administration. In conclusion, amniotic fluid AVP levels can affect fetal plasma AVP concentration, and AVP absorbed from the amniotic fluid by the fetus remains biologically active.

Atrial natriuretic factor and renal function during head-out water immersion in conscious dogs

1986 ◽  
Vol 251 (5) ◽  
pp. R1000-R1004
Author(s):  
K. Miki ◽  
G. Hajduczok ◽  
M. R. Klocke ◽  
J. A. Krasney ◽  
S. K. Hong ◽  
...  
Keyword(s):  
Sodium Excretion ◽  
Atrial Natriuretic Factor ◽  
Time Course ◽  
Water Immersion ◽  
Base Line ◽  
Peripheral Tissues ◽  
Natriuretic Factor ◽  
Peak Value ◽  
Atrial Natriuretic

The potential role of atrial natriuretic factor (ANF) in the renal response to head-out water immersion (WI) was studied. Five female mongrel dogs, trained to stand for 100 min in air followed by 100 min of thermoneutral WI at 37 degrees C or 200 min in air (timed control, TC), were chronically instrumented with arterial and venous catheters. The animals were hydrated with a volume of 0.45% NaCl solution equivalent to 2% of their body weight. Prehydration levels of arterial ANF were 243 +/- 15 (SE), and venous ANF levels were 211 +/- 21 pg/ml. WI resulted in an increase in urine flow from 0.7 +/- 0.1 ml/min to a peak flow of 2.2 +/- 0.3 ml/min (P less than 0.05). On immersion, plasma venous and arterial ANF levels increased significantly by 29 and 21% from the preimmersion values of 183 +/- 14 and 222 +/- 20 pg/ml, respectively. The arterial-venous difference for plasma ANF was maintained at 35 +/- 14 pg/ml (P less than 0.05) during WI; therefore venous sampling may suffice as a measure of circulating ANF levels. Sodium excretion increased linearly during WI to a peak value of 228 +/- 32 mu eq/min from a base line of 52 +/- 12 mu eq/min (P less than 0.05). These data indicate that peripheral tissues extract ANF and that WI is a physiological stimulus for the release of ANF. However, the time course and magnitude of the changes in plasma ANF and urine sodium excretion during WI are not comparable, and other mechanisms are likely responsible for the WI natriuresis.(ABSTRACT TRUNCATED AT 250 WORDS)

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

1991 ◽  
Vol 128 (2) ◽  
pp. 245-248 ◽  
Author(s):  
Kunikazu Kondo ◽  
Takashi Murase ◽  
Kazuo Otake ◽  
Masafumi Ito ◽  
Yutaka Oiso
Keyword(s):  
Arginine Vasopressin ◽  
Vasopressin Release ◽  
Conscious Rats

Vasopressin increases cytosolic free calcium in LLC-PK1 cells through a V1-receptor

1987 ◽  
Vol 253 (2) ◽  
pp. F328-F332 ◽  
Author(s):  
M. A. Burnatowska-Hledin ◽  
W. S. Spielman
Keyword(s):  
Parathyroid Hormone ◽  
Arginine Vasopressin ◽  
Calcium Concentration ◽  
Mdck Cells ◽  
Free Calcium ◽  
Base Line ◽  
Cytosolic Free Calcium ◽  
Free Calcium Concentration ◽  
Cytosolic Free Calcium Concentration ◽  
Dose Dependent

We examined the effects of arginine vasopressin (AVP), parathyroid hormone (PTH), and bradykinin (BK) on the cytosolic free calcium concentration ([Ca]i) in cultured LLC-PK1 and MDCK kidney cell lines by use of the fluorescent Ca chelator fura-2. In LLC-PK1 cells, the addition of AVP but not [1-desamino-8-D-arginine]vasopressin (dDAVP, V2 agonist), PTH, or BK (10(-6) M) caused a significant increase in [Ca]i. The AVP-induced increase in [Ca]i from 61 +/- 6 to 225 +/- 44 nM (n = 7, P less than 0.01) was rapid and transient, returning to base line in 2 to 3 min. The effect of AVP was dose dependent and was present at 1 (61% increase) but not 5 min after extracellular Ca was removed. The effect of 10(-6) M AVP could be blocked with the pressor (V1) antagonist, d(CH2)5Tyr(Me)AVP, but not dDAVP. In MDCK cells, BK, but not AVP and PTH, increased [Ca]i from 146 +/- 11 to 281 +/- 31 nM (n = 9, P less than 0.001). The removal of extracellular Ca (5 min), reduced but did not abolish this effect. These results indicate that [Ca]i mobilized by activation of V1-receptors may mediate AVP-regulated function in some transporting epithelia.

Sign in / Sign up

Export Citation Format

Share Document