scholarly journals Aquaporins, Vasopressin, and Aging: Current Perspectives

Endocrinology ◽  
2015 ◽  
Vol 156 (3) ◽  
pp. 777-788 ◽  
Author(s):  
Grazia Tamma ◽  
Nandu Goswami ◽  
Johannes Reichmuth ◽  
Natale G. De Santo ◽  
Giovanna Valenti

Abstract Functioning of the hypothalamic-neurohypophyseal-vasopressin axis is altered in aging, and the pathway may represent a plausible target to slow the process of aging. Arginine vasopressin, a nine-amino acid peptide that is secreted from the posterior pituitary in response to high plasma osmolality and hypotension, is central in this pathway. Vasopressin has important roles in circulatory and water homoeostasis mediated by vasopressin receptor subtypes V1a (vascular), V1b (pituitary), and V2 (vascular, renal). A dysfunction in this pathway as a result of aging can result in multiple abnormalities in several physiological systems. In addition, vasopressin plasma concentration is significantly higher in males than in females and vasopressin-mediated effects on renal and vascular targets are more pronounced in males than in females. These findings may be caused by sex differences in vasopressin secretion and action, making men more susceptible than females to diseases like hypertension, cardiovascular and chronic kidney diseases, and urolithiasis. Recently the availability of new, potent, orally active vasopressin receptor antagonists, the vaptans, has strongly increased the interest on vasopressin and its receptors as a new target for prevention of age-related diseases associated with its receptor-altered signaling. This review summarizes the recent literature in the field of vasopressin signaling in age-dependent abnormalities in kidney, cardiovascular function, and bone function.

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.


1988 ◽  
Vol 117 (1) ◽  
pp. 59-64 ◽  
Author(s):  
A. Rijnberk ◽  
W. J. Biewenga ◽  
J. A. Mol

Abstract. Two dogs with hyponatremia due to inappropriate arginine vasopressin (AVP) secretion are described. Threshold and sensitivity of AVP secretion were investigated by increasing plasma osmolality with hypertonic saline infusion. In one dog, osmoregulation of AVP secretion occurred at normal sensitivity but at a low threshold. The other dog had a relatively high plasma AVP concentration under (resting) hypotonic conditions with an otherwise normal response to increasing plasma tonicity. In the absence of evidence for associated disease, it is suggested that both dogs have an idiopathic form of the syndrome of inappropriate AVP secretion.


1991 ◽  
Vol 260 (3) ◽  
pp. R533-R539 ◽  
Author(s):  
C. J. Thompson ◽  
P. Selby ◽  
P. H. Baylis

We have studied the reproducibility of the thirst and arginine vasopressin (AVP) responses to osmotic and hypoglycemic stimulation in healthy volunteers undergoing repeat hypertonic (855 mmol/l) saline infusion and insulin tolerance tests (ITTs). Hypertonic saline infusion caused similar mean rises in plasma osmolality, AVP, and thirst on each occasion. Linear-regression analysis defined close relationships between the slopes (r = +0.72, P less than 0.05) and the abscissal intercepts (r = +0.89, P less than 0.001) of the regression lines relating plasma osmolality (Posmol) and plasma AVP (PAVP), and the group intraindividual component of the variance for the slopes and intercepts was 7 and 0.6%, respectively. There were close correlations between the slopes (r = +0.79, P less than 0.02) and the intercepts (r = +0.84, P less than 0.01) of the regression lines relating Posmol and thirst, and group intraindividual component of the variance was 14 and 0.7%, respectively. Hypertonic saline infusion was infused on four occasions in four subjects, and the results showed that the linear regression lines relating PAVP and Posmol and thirst and Posmol were reproducible within an individual. There were similar falls in blood glucose and elevations in PAVP in both ITTs. No relationship was defined between the fall in blood glucose and either the rise in PAVP or the area under the AVP curve (AUC). The intraindividual component of the variance for the rise in AVP and the AUC was 77 and 22.5%, respectively. The AVP and thirst responses to osmotic stimulation are highly reproducible, but there is considerable intraindividual variation in the AVP response to hypoglycemia.


1986 ◽  
Vol 250 (4) ◽  
pp. E352-E361 ◽  
Author(s):  
W. M. Barron ◽  
J. Schreiber ◽  
M. D. Lindheimer

Effects of sex steroids on osmoregulation were studied in intact and ovariectomized Sprague-Dawley rats treated for 2 wk with subcutaneously implanted hormone pellets containing 0.5 mg 17 beta-estradiol (E2) alone (group 1) or combined with 50 mg progesterone (PG; group 2) and 5.0 mg E2 alone (group 3) combined with PG (group 4). An additional group (5) of animals was given 14 daily injections with 100 micrograms/100 g body weight of E2. Controls for each group received vehicle alone. There were no alterations in basal plasma osmolality (Posmol) or vasopressin (PAVP), except for group 3 in which a small (2.5 mosmol/kg) decrement in Posmol was observed. However, mean PNa was decreased (0.9-3.4 meq/l) in hormone-treated rats, and alterations in Pglucose and/or Purea could not explain the Na-osmolal discrepancy. Intraperitoneal hypertonic saline resulted in stepwise increases in both Posmol and PAVP. Regression analysis of PAVP on Posmol demonstrated similar osmotic thresholds for AVP release in estrogen and control rats, but the slope (sensitivity of the response) was significantly (P less than 0.005) greater in hormone-treated animals. In contrast, the PAVP response to isosmotic volume depletion was not altered by estrogen. The enhanced response to osmotic stimuli could not be explained by alterations in plasma volume or pituitary AVP content and differed from PAVP -Posmol relationships observed by us previously in gravid rats. In other experiments Posmol and PAVP were similar during all stages of the estrus cycle, while Posmol was approximately equal to 10 mosmol/kg lower in 21-day gravid rats. These data demonstrate that, although estradiol has little effect on basal osmoregulation or hemodynamically mediated AVP release, PAVP responses to osmotic stimuli are markedly enhanced. These osmoregulatory effects, however, differ from those observed during rodent gestation.


Author(s):  
E. Grazzini ◽  
G. Boccara ◽  
D. Joubert ◽  
M. Trueba ◽  
T. Durroux ◽  
...  

1984 ◽  
Vol 246 (1) ◽  
pp. F105-F109 ◽  
Author(s):  
J. M. Davison ◽  
E. A. Gilmore ◽  
J. Durr ◽  
G. L. Robertson ◽  
M. D. Lindheimer

Osmoregulation was studied in eight women during late pregnancy and again 8-10 wk postpartum. Base-line plasma osmolality (Posmol) was significantly lower during (280.9 +/- 2.1 mosmol/kg, SD) than after (289.4 +/- 2.1 mosmol/kg) pregnancy yet 24-h urinary volume and plasma arginine vasopressin (PAVP) measured in vasopressinase-inactivated blood was similar in both groups (pregnancy, 1.39 +/- 0.56 pg/ml; postpartum, 1.25 +/- 0.62 pg/ml). After 12 h of dehydration PAVP rose similarly and significantly both during (2.25 +/- 0.81 pg/ml) and after (2.89 +/- 1.19 pg/ml) gestation, and Uosmol was similar on both occasions (pregnancy, 779 +/- 121 mosmol/kg; postpartum, 784 +/- 102 mosmol/kg). When Posmol was increased by the slow infusion of 5% saline PAVP increased as soon as body tonicity did both during and after pregnancy. PAVP correlated significantly with Posmol in each subject (range of r, 0.75-0.99) and the mean regression lines [pregnancy, PAVP = 0.32 (Posmol; -279), r = 0.79; postpartum, PAVP = 0.38 (Posmol, -285), r = 0.86] demonstrated that the apparent osmotic threshold for AVP secretion was 6 mosmol/kg lower during than after gestation. Similarly the Posmol at which the subject experienced a conscious desire to drink was lower in pregnant (287 +/- 1.6 mosmol/kg) compared with postpartum subjects (298 +/- 2.0 mosmol/kg; P less than 0.001). These data demonstrate decreased osmotic thresholds for AVP release and thirst during human pregnancy and explain why gravidas can maintain their new lower Posmol within narrow limits.


2005 ◽  
Vol 5 (5) ◽  
pp. 562-567 ◽  
Author(s):  
Wilson Abrao Saad . ◽  
Luiz Antonio de Arru . ◽  
Jose Antunes-Rodrigu . ◽  
William Abrao Saad . ◽  
Ismael Franscisco Mo . ◽  
...  

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.


1987 ◽  
Vol 252 (6) ◽  
pp. R1138-R1142 ◽  
Author(s):  
C. J. Thompson ◽  
J. M. Burd ◽  
P. H. Baylis

Drinking rapidly abolishes thirst and vasopressin secretion in dehydrated humans before major changes in plasma osmolality are observed. We studied the effects of drinking on plasma vasopressin and thirst in seven healthy volunteers rendered hypernatremic by the infusion of hypertonic (855 mmol/l) sodium chloride solution. Thirst was measured on a visual analogue scale (0-10 cm). Infusion of hypertonic saline caused linear increases in plasma osmolality (289 +/- 1 to 306 +/- 1 mosmol/kg, mean +/- SE, P less than 0.001), plasma vasopressin (0.6 +/- 0.2 to 6.4 +/- 1.9 pmol/l, P less than 0.001), and thirst (1.4 +/- 0.4 to 7.4 +/- 0.5 cm, P less than 0.001). Water was allowed 15 min after cessation of the infusion, and within 5 min of drinking both plasma vasopressin and thirst were significantly lower than postinfusion. After 20 min of drinking, plasma vasopressin had fallen from 6.5 +/- 0.9 to 1.3 +/- 0.3 pmol/l (P less than 0.001) and thirst from 7.7 +/- 0.5 to 1.0 +/- 0.2 cm (P less than 0.001) despite no significant change in plasma osmolality (306 +/- 0.9 to 304 +/- 0.8 mosmol/kg, P = 0.17), and the drinking of 1,200 +/- 60 ml of water, over 85% of the mean cumulative water intake in the 30-min drinking period. Control studies in the same subjects showed comparable rises in plasma vasopressin, plasma osmolality, and thirst during hypertonic saline infusion but no fall in any of these parameters during an equivalent 30-min period after the infusions, during which water was withheld.(ABSTRACT TRUNCATED AT 250 WORDS)


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