Immersion diuresis without expected suppression of vasopressin

1984 ◽  
Vol 57 (1) ◽  
pp. 123-128 ◽  
Author(s):  
S. E. Kravik ◽  
L. C. Keil ◽  
J. E. Silver ◽  
N. Wong ◽  
W. A. Spaul ◽  
...  

To investigate fluid, electrolyte, and plasma vasopressin (PVP) and renin activity (PRA) responses, six men (20–35 yr) were immersed to the neck (NI) in water at 34.5 degrees C for six h after overnight food and fluid restriction. Diuresis was 1,061 +/- 160 (SE) ml/6 h during immersion and water balance was -1,285 +/- 104 ml/6 h. Preimmersion PVP was 0.7 +/- 0.2 pg/ml and increased to 3.0 +/- 0.6 pg/ml (P less than 0.05) at 6 h. PVP was unchanged at 1.2 +/- 0.1 pg/ml in the 6-h seated nonimmersionexperiment at 25 degrees C. Plasma volume increased by 7.8 +/- 1.6% (P less than 0.05) at 60 min of NI and decreased thereafter. Serum osmolality was constant (292 +/- 1 mosmol/kg) throughout NI, whereas PRA decreased progressively from 1.9 to 0.5 ng angiotensin I X ml-1 X h-1 (P less than 0.05) at theend of immersion. In spite of moderate thirst just before NI, thirst sensations were attenuated and no water was consumed ad libitum during immersion. These data indicate that PVP is not suppressed whenthere is no fluid intake during immersion and suggest that the action of factors other than PVP suppression are necessary to explain the mechanism of immersion diuresis.

1994 ◽  
Vol 267 (5) ◽  
pp. R1168-R1173 ◽  
Author(s):  
R. L. Thunhorst ◽  
M. Morris ◽  
A. K. Johnson

Simultaneous administration of the diuretic furosemide (10 mg/kg) and a low dose of the angiotensin-converting enzyme (ACE) inhibitor captopril (5 mg/kg) results in short-latency thirst and sodium appetite (i.e., the rapid ingestion of water and NaCl solution). To elucidate potential mechanisms for mediating this behavior, changes in plasma levels of key hormones involved in fluid intake and balance were characterized in rats subjected to this treatment protocol. Rats treated jointly with furosemide and low-dose captopril had exaggerated increases in plasma renin activity and angiotensin I but equivalent increases in plasma aldosterone compared with rats treated with either agent alone. Treatment with furosemide plus low-dose captopril increased plasma vasopressin but not plasma oxytocin. The administration of a higher dose of captopril (100 mg/kg) with furosemide, a combination of drugs that does not stimulate fluid intake (29), further increased plasma renin activity and angiotensin I but prevented the rise in plasma vasopressin. The results support the hypothesis that thirst and salt appetite generated by this protocol depend on angiotensin II formed within brain circumventricular organs rather than the systemic circulation.


1983 ◽  
Vol 55 (6) ◽  
pp. 1688-1693 ◽  
Author(s):  
J. E. Greenleaf ◽  
J. T. Morse ◽  
P. R. Barnes ◽  
J. Silver ◽  
L. C. Keil

To investigate changes in plasma volume (PV) and osmolality as stimuli for plasma vasopressin (PVP) suppression and diuresis, seven normal healthy men (22-48 yr) were immersed to the neck for 4 h in a sitting position in tap water (34.5 degrees C) after overnight food and fluid restriction. Mean +/- SE urine volume was 823 +/- 123 ml/4 h; fluid intake was 400 ml/4 h, and mean negative water balance was 944 ml/4 h. Urinary sodium excretion increased from 0.77 to 1.25 mosmol/min (P less than 0.05) and UNaV from 0.14 to 0.37 meq/min (P less than 0.05). During immersion, PV (T-1824) increased by 8.8% (P less than 0.05) during the first 30 min and declined linearly thereafter. Mean +/- SD serum osmolality (294 +/- 1.2 mosmol/kg H2O) and sodium (143.2 +/- 0.4 meq/l) were constant throughout immersion; PVP (2.3 +/- 0.5 pg/ml) and plasma renin activity [0.3 +/- 0.2 ng ANG I/(ml X h]) were not significantly changed. Thus, the composition of the fluid entering the vascular space maintained constant serum osmolality and PVP throughout immersion. These findings do not support the hypothesis that acute expansion of central volume and PV cause suppression of PVP. The results suggest a mechanism other than or in addition to PVP suppression as a contributory cause of the immersion diuresis.


1976 ◽  
Vol 45 (4) ◽  
pp. 432-436 ◽  
Author(s):  
Henry A. Shenkin ◽  
Honorio S. Bezier ◽  
William F. Bouzarth

✓ Water balance studies in postcraniotomy patients indicate that restriction of fluid intake to 1 liter daily maintains the patient in homeostatic balance. A larger fluid intake will expand the extracellular space and presumably unfavorably influence cerebral edema. Daily observation of serum sodium and osmolarity and blood urea nitrogen, and preserving their normalcy, is a rational way of regulating fluid intake of the brain-injured patient. Fluid restriction should be used with caution if hyperosmolar agents, diuretics, or dexamethasone are also administered.


1986 ◽  
Vol 61 (4) ◽  
pp. 1410-1417 ◽  
Author(s):  
M. H. Harrison ◽  
L. C. Keil ◽  
C. A. Wade ◽  
J. E. Silver ◽  
G. Geelen ◽  
...  

To determine the effect of hydration on the early osmotic and intravascular volume and endocrine responses to water immersion the hematocrit, hemoglobin, plasma renin activity (PRA), and plasma electrolyte, aldosterone (PA), and vasopressin (PVP) concentrations were measured during immersion following 24-h dehydration; these were compared with corresponding values following rapid rehydration. Six men and one woman (age 23–46 yr) underwent 45 min of standing immersion to the neck preceded by 45-min standing without immersion, first dehydrated, and then 105 min later after rehydration with water. Immersion caused an isotonic expansion of the plasma volume (P less than 0.001), which occurred independently of hydration status. Suppression of PRA (P less than 0.001) and PA (P less than 0.001) during both immersions also occurred independently of hydration status. Suppression of plasma vasopressin was observed during dehydrated immersion (P less than 0.001) but not during rehydrated immersion. It is concluded that plasma tonicity is not a factor influencing PVP suppression during water immersion.


1997 ◽  
Vol 22 (1) ◽  
pp. 48-57 ◽  
Author(s):  
Jan M. Schroeder ◽  
Kris L. Heck ◽  
Jeffrey A. Potteiger

The effectiveness of a new water delivery system (the Water-Del) was examined for maintaining euhydration compared to other fluid replacement strategies. Subjects (N = 10) performed three 60-min cycling trials (@ 50% of VO2max) in an environmental chamber (27 °C; RH = 50%). Trials were randomly assigned from Water-Del (metered: 200 ml water every 15 min), ad libitum every 15 min (ad-lib-15), and ad libitum (ad-lib). Total water intake (TWI), changes in plasma volume (ΔPV), body Weight (ΔBW), thirst, skin temperature (Tsk), and heart rate (HR) were measured. A significant difference (p ≤.05) among trials was observed for TWI, with metered (1.200 ± 0.12 ml) being greater than ad-lib-15 (358 ± 48 ml) and ad-lib (522 ± 106 ml). No significant difference was found for ΔPV. A significant difference (p ≤.05) for ΔHW was observed with metered (0.28 ± 0.16 kg) being different than ad-lib-l5 (−0.63 ± 0.12 kg) and ad-lib (−0.34 ± 0.14 kg). No significant differences (p > .05) were found for thirst, Tsk, or HR. The Water-Del provides for greater fluid intake during exercise compared to other replacement strategies. Key words: hydration, dehydration, plasma volume


1986 ◽  
Vol 61 (2) ◽  
pp. 766-774 ◽  
Author(s):  
S. E. Kravik ◽  
L. C. Keil ◽  
G. Geelen ◽  
C. E. Wade ◽  
P. R. Barnes ◽  
...  

Blood pressure, pulse rate (PR), serum osmolality and electrolytes, as well as plasma vasopressin (PVP) and plasma renin activity (PRA), were measured in five men and two women [mean age 38.6 +/- 3.9 (SE) yr] before, during, and after inflation of an antigravity suit that covered the legs and abdomen. After 24 h of fluid deprivation the subjects stood quietly for 3 h: the 1st h without inflation, the 2nd with inflation to 60 Torr, and the 3rd without inflation. A similar control noninflation experiment was conducted 10 mo after the inflation experiment using five of the seven subjects except that the suit was not inflated during the 3-h period. Mean arterial pressure increased by 14 +/- 4 (SE) Torr (P less than 0.05) with inflation and decreased by 15 +/- 5 Torr (P less than 0.05) after deflation. Pulse pressure (PP) increased by 7 +/- 2 Torr (P less than 0.05) with inflation and PR decreased by 11 +/- 5 beats/min (P less than 0.05); PP and PR returned to preinflation levels after deflation. Plasma volume decreased by 6.1 +/- 1.5% and 5.3 +/- 1.6% (P less than 0.05) during hours 1 and 3, respectively, and returned to base line during inflation. Inflation decreased PVP from 6.8 +/- 1.1 to 5.6 +/- 1.4 pg/ml (P less than 0.05) and abolished the significant rise in PRA during hour 1. Both PVP and PRA increased significantly after deflation: delta = 18.0 +/- 5.1 pg/ml and 4.34 +/- 1.71 ng angiotensin I X ml-1 X h-1, respectively. Serum osmolality and Na+ and K+ concentrations were unchanged during the 3 h of standing.(ABSTRACT TRUNCATED AT 250 WORDS)


1984 ◽  
Vol 247 (6) ◽  
pp. R968-R971 ◽  
Author(s):  
G. Geelen ◽  
L. C. Keil ◽  
S. E. Kravik ◽  
C. E. Wade ◽  
T. N. Thrasher ◽  
...  

To study the effects of nonosmotic and nonvolumetric factors that may influence secretion of vasopressin, serum Na+, K+, and osmolality (Osm), hemoglobin, hematocrit, plasma arginine vasopressin (AVP), aldosterone (PA), and renin activity (PRA) were measured in five men and three women (26–50 yr, 73 +/- 4 kg) before and after 24 h of mild dehydration (food but no fluid) and seven times during the 1st h after rehydration with 10 ml/kg of tap water (17.5 +/- 0.5 degrees C) consumed in 105 s (range 35-240 s). Dehydration increased mean serum Na+ 3.7 +/- 0.7 meq/l (P less than 0.05), osmolality 9.1 +/- 1.1 mosmol/kg (P less than 0.05), and AVP from a hydrated level of 1.7 +/- 0.2 to 3.3 +/- 0.5 pg/ml (delta = 1.6 pg/ml, P less than 0.05). After rehydration AVP fell to 2.4 +/- 0.3 pg/ml (P less than 0.05) within 3 min and reached the water-replete level of 1.8 +/- 0.3 pg/ml 9 min after drinking started. Serum Na+ and Osm did not change until 30–60 min after drinking. No significant changes occurred in PRA, hemogloblin, hematocrit, or calculated delta in plasma volume, but PA increased from 11.1 +/- 1.5 ng/dl after dehydration to 15.6 +/- 2.6 ng/dl (P less than 0.05) between 30 and 60 min after drinking. The rapid fall in plasma AVP after rehydration took place in the absence of the expected changes in the primary regulators of plasma AVP (i.e., osmolality and plasma volume), with no change in blood pressure. The results suggest that oropharyngeal factors, alone or combined with gastric stimuli, are implicated.


2013 ◽  
Vol 23 (6) ◽  
pp. 545-553 ◽  
Author(s):  
Lewis J. James ◽  
Susan M. Shirreffs

Weight categorized athletes use a variety of techniques to induce rapid weight loss (RWL) in the days leading up to weigh in. This study examined the fluid and electrolyte balance responses to 24-hr fluid restriction (FR), energy restriction (ER) and fluid and energy restriction (F+ER) compared with a control trial (C), which are commonly used techniques to induce RWL in weight category sports. Twelve subjects (six male, six female) received adequate energy and water (C) intake, adequate energy and restricted water (~10% of C; FR) intake, restricted energy (~25% of C) and adequate water (ER) intake or restricted energy (~25% of C) and restricted (~10% of C) water intake (F+ER) in a randomized counterbalanced order. Subjects visited the laboratory at 0 hr, 12 hr, and 24 hr for blood and urine sample collection. Total body mass loss was 0.33% (C), 1.88% (FR), 1.97% (ER), and 2.44% (F+ER). Plasma volume was reduced at 24 hr during FR, ER, and F+ER, while serum osmolality was increased at 24 hr for FR and F+ER and was greater at 24 hr for FR compared with all other trials. Negative balances of sodium, potassium, and chloride developed during ER and F+ER but not during C and FR. These results demonstrate that 24 hr fluid and/or energy restriction significantly reduces body mass and plasma volume, but has a disparate effect on serum osmolality, resulting in hypertonic hypohydration during FR and isotonic hypohydration during ER. These findings might be explained by the difference in electrolyte balance between the trials.


1984 ◽  
Vol 67 (4) ◽  
pp. 413-420 ◽  
Author(s):  
Sming Kaojarern ◽  
Polavat Chennavasin ◽  
Ann Burdette ◽  
William B. Campbell ◽  
D. Craig Brater

1. Eight normal subjects underwent water loading alone and water loading plus 40 mg of frusemide IV, fluid intake ad libitum alone and fluid intake ad libitum plus frusemide, plus each of the preceding after pretreatment with indomethacin. 2. After frusemide administration, increases in urinary sodium excretion paralleled increases in urinary volume, and urinary prostaglandin E2 (PGE2) excretion correlated closely with sodium excretion (y = 1.03x −0.28; r = 0.940; P<.0001). 3. In the absence of the diuretic, urinary volume varied over a wide range with little change in sodium excretion. Again, urinary PGE2 excretion correlated with urinary sodium excretion (y = 0.12x + 0.05; r = 0.789; P<.002). However, the correlation differed markedly from that observed in the studies with frusemide. 4. Expressing urinary PGE2 excretion as a function of urinary volume for all of the studies resulted in a highly significant correlation (y = 10.7x −0.70; r = 0.975; P<.0001). 5. Multiple and stepwise regression analyses assessing the correlation of urinary PGE2 excretion with urinary flow rate and with indices of function of various nephron segments indicate that the correlation with urinary PGE2 could be predominantly accounted for by urinary volume. 6. We conclude that in the condition of this study in man, urinary PGE2 excretion is a correlate of urinary volume.


1995 ◽  
Vol 19 (3) ◽  
pp. 759-762 ◽  
Author(s):  
Hanna Taivainen ◽  
Kalevi Laitinen ◽  
Riitta Tahtela ◽  
Kalervo Kiianmaa ◽  
Matti J. Valimaki

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