scholarly journals Acute Increases in Water Consumption Supress Copeptin in Low Drinkers

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 1389-1389
Author(s):  
Abigail Colburn ◽  
Adam Seal ◽  
HyunGyu Suh ◽  
Stavros Kavouras

Abstract Objectives To assess the acute effect of adequate water consumption on copeptin, a marker of arginine vasopressin, in low drinkers. Methods Six healthy (5 males, 1 female) low drinkers (age 43 ± 7 y, BMI 30.5 ± 3) were recruited based on self-reported daily water consumption ≤1.5 L·day−1 in males or 1.0 L·day−1 in females (854 ± 432 mL·d−1) and 24-h urine osmolality ≥800 mmol·kg−1 (968 ± 114 mmol·kg−1). Participants completed two counterbalanced crossover 11-h protocols. They were provided either the Institute of Medicine's recommended amount of water excluding food (males: 3 L, females: 2 L, HWI) or an amount representing the bottom quartile of water consumption observed in the National Health and Nutrition Examination Survey (males: 0.5 L, females: 0.4 L, LWI). Food was provided to participants and standardized to body weight (100 kJ·Kg−1) using a consistent ratio of macronutrients. Blood samples were collected at hours 700, 800, 900, 1200, 1300, 1400, 1600, 1700, and 1800. Results There was a significant main effect of water intake on plasma osmolality (F = 11.838, P = 0.018) with greater values in LWI at 1200 (HWI: 287 ± 3, LWI: 291 ± 3; P = 0.013), 1400 (HWI: 287 ± 4, LWI: 291 ± 5; P = 0.049), and 1700 (HWI: 287 ± 2, LWI: 292 ± 4; P = 0.004). There was also a significant main effect of water intake on copeptin (F = 9.848, P = 0.026) with higher values in LWI at 0800 (HWI: 6.1 ± 2.3, LWI: 8.7 ± 3.7; P = 0.016), 0900 (HWI: 5.3 ± 2.4, LWI: 9.2 ± 4.5; P = 0.013), 1200 (HWI: 4.2 ± 1.9, LWI: 7.8 ± 4.6; P = 0.021), 1400 (HWI: 4.3 ± 1.8, LWI: 8.3 ± 4.7; P = 0.033), 1600 (HWI: 4.7 ± 2.5, LWI: 7.6 ± 4.5; P = 0.049), and 1800 (HWI: 4.4 ± 2.5, LWI: 7.8 ± 5.2; P = 0.048). Water intake did not influence change in plasma volume (P = 0.214). Conclusions Copeptin was suppressed in response to acute increases in water consumption via suppression of plasma osmolality. Copeptin may serve as a sensitive marker for changes in total water intake. Funding Sources This study was supported by Arizona State University College of Health Solutions.

Author(s):  
R.A. Cooper ◽  
Bryany Hill ◽  
J.A. Kirk

It is commonly held that goats prefer their water ‘warm’ and that consumption may be encouraged by offering warmed water. Conversely, it is argued that water intake may go down if water is ‘too cold.’ There are, however, few data available and no definition of what constitutes ‘warm’ or ‘cold’ in the eyes of a goat. This trial was undertaken to provide some data in an attempt to confirm or refuse these conventional wisdoms.


2015 ◽  
Vol 41 (3) ◽  
pp. 248-256 ◽  
Author(s):  
Niek F. Casteleijn ◽  
Debbie Zittema ◽  
Stephan J.L. Bakker ◽  
Wendy E. Boertien ◽  
Carlo A. Gaillard ◽  
...  

Background: Vasopressin plays an essential role in osmoregulation, but has deleterious effects in patients with ADPKD. Increased water intake to suppress vasopressin activity has been suggested as a potential renoprotective strategy. This study investigated whether urine and plasma osmolality can be used as reflection of vasopressin activity in ADPKD patients. Methods: We measured urine and plasma osmolality, plasma copeptin concentration, total kidney volume (TKV, by MRI) and GFR (125I-iothalamate). In addition, change in estimated GFR (eGFR) during follow-up was assessed. Results: Ninety-four patients with ADPKD were included (56 males, age 40 ± 10, mGFR 77 ± 32 ml/min/1.73 m2, TKV 1.55 (0.99-2.40) l. Urine osmolality, plasma osmolality and copeptin concentration were 420 ± 195, 289 ± 7 mOsmol/l and 7.3 (3.2-14.6) pmol/l, respectively. Plasma osmolality was associated with copeptin concentration (R = 0.54, p < 0.001), whereas urine osmolality was not (p = 0.4). In addition, urine osmolality was not associated with TKV (p = 0.3), in contrast to plasma osmolality (R = 0.52, p < 0.001) and copeptin concentration (R = 0.61, p < 0.001). Fifty-five patients were followed for 2.8 ± 0.8 years. Baseline plasma and urine osmolality were not associated with change in eGFR (p = 0.6 and p = 0.3, respectively), whereas baseline copeptin concentration did show an association with change in eGFR, in a crude analysis (St. β = -0.41, p = 0.003) and also after adjustment for age, sex and TKV (St. β = -0.23, p = 0.05). Conclusions: These data suggest that neither urine nor plasma osmolality are valid measures to identify ADPKD patients that may benefit from increasing water intake. Copeptin appears a better alternative for this purpose.


1986 ◽  
Vol 251 (3) ◽  
pp. R621-R626
Author(s):  
R. G. Park ◽  
M. Congiu ◽  
D. A. Denton ◽  
M. J. McKinley

The contribution of extracellular fluid volume (ECFV) to water consumption and plasma vasopressin concentration (PAVP) after water deprivation for 52 h was examined in sheep. Intravenous infusion of isotonic NaCl, equivalent to either estimated ECFV loss or total body water loss, significantly reduced water intake by 37% when water was offered 3 h after infusion but not when water was offered 1 h after infusion. Plasma osmolality (POsm) was reduced after 3 h. Infusion of 200 mM NaCl, which maintained POsm, decreased water consumption by the same degree as isotonic NaCl infusion. Thus large decreases in POsm had no effect on water intake in this experimental protocol. Lack of inhibition of drinking 1 h after infusion suggests that the decrease observed after 3 h may have been mediated by receptors in the interstitial fluid (ISF) compartment and not the intravascular compartment. PAVP was reduced 3 h after infusion of NaCl but not at 1 or 2 h after infusion. POsm was also decreased at 3 h. Thus reduction of PAVP by NaCl infusion may have been caused by either ISF or intracellular fluid volume expansion.


2018 ◽  
Vol 72 (Suppl. 2) ◽  
pp. 21-27 ◽  
Author(s):  
Sofia Enhörning ◽  
Olle Melander

Background: Type 2 diabetes, chronic kidney disease (CKD) and its cardiovascular complications are increasing as health problems worldwide. These diseases are interrelated with overlapping occurrence and once diabetes is established, the risk of cardiorenal disease is dramatically elevated. Thus, a search for unifying modifiable risk factors is key for effective prevention. Summary: Elevated fasting plasma concentration of vasopressin, measured with the marker copeptin, predicts new onset type 2 diabetes as well as renal function decline. Furthermore, we recently showed that increased plasma copeptin concentration independently predicts the development of both CKD and other specified kidney diseases. In consequence, high copeptin is an independent risk factor for cardiovascular disease and premature mortality in both diabetes patients and in the general population. Vasopressin is released when plasma osmolality is high, and the easiest way to lower plasma vasopressin and copeptin concentration is to increase water intake. In a human water intervention experiment with 1 week of 3 L/day increased water intake, the one third of the participants with the greatest copeptin reduction (water responders) were those with a phenotype of low water intake (high habitual plasma copeptin and urine osmolality, and low urine volume). The water-responders had a copeptin reduction of 41% after 1 week of increased water intake compared to a control week; in contrast, a 3% reduction occurred in the other two thirds of the study participants. Among water responders, increased water intake also induced a reduction in fasting glucagon concentration. Key Messages: Elevated copeptin, a measure of vasopressin, is a risk marker of metabolic and cardiorenal diseases and may assist in the detection of individuals at higher risk for these diseases. Furthermore, individuals with high copeptin and other signs of low water intake may experience beneficial glucometabolic effects of increased water intake. Future randomized control trials investigating effects of hydration on glucometabolic and renal outcomes should focus on individuals with signs of low water intake including high plasma copeptin concentration.


1987 ◽  
Vol 65 (10) ◽  
pp. 2142-2146 ◽  
Author(s):  
R. L. Kline ◽  
K.-Y. Chow ◽  
P. F. Mercer

Vasopressin (AVP) in acute experiments has been shown to influence cardiovascular reflexes, but the effect of a more prolonged administration of AVP on the sympathetic nervous system has not been investigated. Long–Evans rats were treated for 7 days with AVP (Pitressin tannate in oil, with single daily doses of 100 or 500 mU∙100 g−1, s.c.) to determine whether AVP alters norepinephrine (NE) turnover in kidney, intestine, or skeletal muscle. Control rats were given equal doses of peanut oil daily. NE turnover was determined by measuring the decline in tissue levels of NE for 8 h after inhibition of tyrosine hydroxylase with α-methyl-p-tyrosine (300 mg∙kg−1, i.p. every 4 h). Measurements of water intake, urine output, and urine osmolality showed that chronic administration of the high dose, but not the low dose, of AVP produced maintained increases in urine osmolality and decreases in water intake and urine output. Body weight, plasma osmolality, plasma electrolytes, and hematocrit were not significantly altered by AVP treatment, but mean arterial pressure was elevated significantly (control, 105 ± 3 mmHg versus AVP, 119 ± 4 mmHg, p < 0.05) (1 mmHg = 133.3 Pa) in the high dose group. Plasma renin activity was decreased slightly, but significantly in rats treated with the high dose of AVP. Compared with results in control animals, there were no statistically significant changes in NE turnover after chronic administration of either the low or the high dose of AVP. The results indicate that administration of AVP for 7 days to rats in normal fluid balance does not result in a decrease in NE turnover in peripheral organs.


1968 ◽  
Vol 46 (6) ◽  
pp. 873-881 ◽  
Author(s):  
Melvin J. Fregly

Exposure of rats to air at 6 °C for 10 days increased food intake and urine output but failed to affect water intake. A comparison of water with food intake revealed a smaller water intake for a given food intake for cold-exposed than for control rats. The urine output at a given water intake was also greater for cold-exposed rats. In addition, cold exposure failed to affect urine osmolality significantly. Thus, the greater solute output accompanying cold exposure was accomplished by increasing urine flow rather than by concentrating urine. These results suggest possible mechanisms for both the relative dehydration and increased plasma osmolality observed after removal of rats from cold air. Both fecal and urinary routes of sodium and potassium excretion were increased by cold exposure; however, fecal excretions of both potassium and sodium were greater fractions of the total output during cold exposure than prior to it. Although cold exposure tends to induce a relative dehydration in rats, an important factor limiting the extent of the dehydration may be increased fecal electrolyte loss.


1992 ◽  
Vol 70 (5) ◽  
pp. 645-650
Author(s):  
L. N. Peterson ◽  
S. Mathur ◽  
J. S. Borzecki

Activation of the renin-angiotensin system induced by feeding a low NaCl, K-free (LS) diet is associated with polydipsia and a chronic reduction in effective plasma osmolality (efPosm). We have recently shown that converting enzyme inhibition with enalapril (EP) abolishes polydipsia. The present study was designed to test the hypothesis that the osmotic threshold for vasopressin is reset in rats fed the LS diet and to examine the effect of EP on ambient and osmotically stimulated plasma vasopressin levels (PAvp). Animals were fed the LS diet or a control salt diet and treated with vehicle or the lowest dose of EP sufficient to prevent polydipsia (7.5 mg∙kg−1∙day−1) in rats fed the LS diet. PAVP and efPosm were measured under ambient conditions and after osmotic loading. Urine osmolality (Uosm) was measured under ambient conditions and after water loading. The chronic reduction in efPosm in LS rats was associated with the excretion of a Uosm 1–2 times greater than the corresponding Posm, PAVP similar to controls (LS, 2.27 ± 1.08 vs. control, 1.19 ± 0.22 pg/mL) and the ability to excrete a water load. Following osmotic loading, efPosm and PAVP increased significantly and similarly in both LS and control rats. EP administration had no effect on water intake, ambient efPosm and PAVP, and the AVP response to osmotic loading in rats fed the control diet. EP prevented polydipsia in LS rats, however it had no significant effect on ambient or osmotically stimulated PAVP or efPosm. These results provide evidence that the osmotic threshold for AVP is reset in rats fed the LS diet and although converting enzyme inhibition has a profound effect on water intake, angiotensin II does not appear to be the only variable affecting the osmotic threshold for AVP release.Key words: arginine vasopressin, antidiuretic hormone, osmotic threshold, plasma osmolality, rats, converting enzyme inhibition, angiotensin II, thirst.


2015 ◽  
Vol 309 (1) ◽  
pp. F48-F56 ◽  
Author(s):  
Nirupama Ramkumar ◽  
Deborah Stuart ◽  
Matias Calquin ◽  
Syed Quadri ◽  
Shuping Wang ◽  
...  

The prorenin receptor (PRR), a recently discovered component of the renin-angiotensin system, is expressed in the nephron in general and the collecting duct in particular. However, the physiological significance of nephron PRR remains unclear, partly due to developmental abnormalities associated with global or renal-specific PRR gene knockout (KO). Therefore, we developed mice with inducible nephron-wide PRR deletion using Pax8-reverse tetracycline transactivator and LC-1 transgenes and loxP flanked PRR alleles such that ablation of PRR occurs in adulthood, after induction with doxycycline. Nephron-specific PRR KO mice have normal survival to ∼1 yr of age and no renal histological defects. Compared with control mice, PRR KO mice had 65% lower medullary PRR mRNA and protein levels and markedly diminished renal PRR immunofluorescence. During both normal water intake and mild water restriction, PRR KO mice had significantly lower urine osmolality, higher water intake, and higher urine volume compared with control mice. No differences were seen in urine vasopressin excretion, urine Na+ and K+ excretion, plasma Na+, or plasma osmolality between the two groups. However, PRR KO mice had reduced medullary aquaporin-2 levels and arginine vasopressin-stimulated cAMP accumulation in the isolated renal medulla compared with control mice. Taken together, these results suggest nephron PRR can potentially modulate renal water excretion.


2014 ◽  
Vol 1 (4) ◽  
pp. 496-499
Author(s):  
Buchineni Madhavulu ◽  
Pathapati Rama Mohan ◽  
, Devaraju Sreebhushan Raju

2016 ◽  
Vol 104 (6) ◽  
pp. 1554-1561 ◽  
Author(s):  
Asher Y Rosinger ◽  
Hannah G Lawman ◽  
Lara J Akinbami ◽  
Cynthia L Ogden

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