Estradiol impairs hyposmoregulatory capacity in the euryhaline tilapia, Oreochromis mossambicus

2001 ◽  
Vol 281 (4) ◽  
pp. R1161-R1168 ◽  
Author(s):  
Mathilakath M. Vijayan ◽  
Akihiro Takemura ◽  
Thomas P. Mommsen

Freshwater (FW)-adapted tilapia ( Oreochromis mossambicus) were treated with estradiol (E2) for 4 days to stimulate protein synthesis and sampled at 0, 4, and 24 h after exposure to 50% seawater (SW). E2 increased circulating vitellogenin (VTG) levels in large amounts, indicative of unusually high rates of hepatic protein synthesis. E2 treatment prevented the recovery of plasma osmolality in 50% SW that was evident in the sham group. Plasma sodium concentration was significantly elevated with E2 in FW, but the levels did not change in 50% SW. Gill Na+-K+-ATPase activity was significantly lower in the E2 group compared with sham-injected tilapia in 50% SW. No significant differences were noted in plasma cortisol, thyroxine, triiodothyronine, or glucose concentration with E2 in 50% SW. E2 significantly lowered several key liver enzyme activities and also decreased gill lactate dehydrogenase and malate dehydrogenase activities over a 24-h period. Together, our results suggest that E2 impairs ion regulation in tilapia, partially mediated by a decreased metabolic capacity in liver and gill. The decreased tissue metabolic capacity is likely due to E2-induced energy repartitioning processes that are geared toward VTG synthesis at the expense of other energy-demanding pathways.

2015 ◽  
Vol 50 (2) ◽  
pp. 141-146 ◽  
Author(s):  
Michael A. McKenney ◽  
Kevin C. Miller ◽  
James E. Deal ◽  
Julie A. Garden-Robinson ◽  
Yeong S. Rhee

Context: Twenty-five percent of athletic trainers administer pickle juice (PJ) to treat cramping. Anecdotally, some clinicians provide multiple boluses of PJ during exercise but warn that repeated ingestion of PJ may cause hyperkalemia. To our knowledge, no researchers have examined the effect of ingesting multiple boluses of PJ on the same day or the effect of ingestion during exercise. Objective: To determine the short-term effects of ingesting a single bolus or multiple boluses of PJ on plasma variables and to characterize changes in plasma variables when individuals ingest PJ and resume exercise. Design: Crossover study. Setting: Laboratory. Patients or Other Participants: Nine euhydrated men (age = 23 ± 4 years, height = 180.9 ± 5.8 cm, mass = 80.7 ± 13.8 kg, urine specific gravity = 1.009 ± 0.005). Intervention(s): On 3 days, participants rested for 30 minutes, and then a blood sample was collected. Participants ingested 0 or 1 bolus (1 mL·kg−1 body weight) of PJ, donned sweat suits, biked vigorously for 30 minutes (approximate temperature = 37°C, relative humidity = 18%), and had a blood sample collected. They either rested for 60 seconds (0- and 1-bolus conditions) or ingested a second 1 mL·kg−1 body weight bolus of PJ (2-bolus condition). They resumed exercise for another 35 minutes. A third blood sample was collected, and they exited the environmental chamber and rested for 60 minutes (approximate temperature = 21°C, relative humidity = 18%). Blood samples were collected at 30 and 60 minutes postexercise. Main Outcome Measure(s): Plasma sodium concentration, plasma potassium concentration, plasma osmolality, and changes in plasma volume. Results: The number of PJ boluses ingested did not affect plasma sodium concentration, plasma potassium concentration, plasma osmolality, or changes in plasma volume over time. The plasma sodium concentration, plasma potassium concentration, and plasma osmolality did not exceed 144.6 mEq·L−1 (144.6 mmol·L−1), 4.98 mEq·L−1 (4.98 mmol·L−1), and 289.5 mOsm·kg−1H2O, respectively, in any condition at any time. Conclusions: Ingesting up to 2 boluses of PJ and resuming exercise caused negligible changes in blood variables. Ingesting up to 2 boluses of PJ did not increase plasma sodium concentration or cause hyperkalemia.


2009 ◽  
Vol 44 (5) ◽  
pp. 454-461 ◽  
Author(s):  
Kevin C. Miller ◽  
Gary Mack ◽  
Kenneth L. Knight

Abstract Context: Health care professionals advocate that athletes who are susceptible to exercise-associated muscle cramps (EAMCs) should moderately increase their fluid and electrolyte intake by drinking sport drinks. Some clinicians have also claimed drinking small volumes of pickle juice effectively relieves acute EAMCs, often alleviating them within 35 seconds. Others fear ingesting pickle juice will enhance dehydration-induced hypertonicity, thereby prolonging dehydration. Objective: To determine if ingesting small quantities of pickle juice, a carbohydrate-electrolyte (CHO-e) drink, or water increases plasma electrolytes or other selected plasma variables. Design: Crossover study. Setting: Exercise physiology laboratory. Patients or Other Participants: Nine euhydrated, healthy men (age  =  25 ± 2 years, height  =  179.4 ± 7.2 cm, mass  =  86.3 ± 15.9 kg) completed the study. Intervention(s): Resting blood samples were collected preingestion (−0.5 minutes); immediately postingestion (0 minutes); and at 1, 5, 10, 15, 20, 25, 30, 45, and 60 minutes postingestion of 1 mL/kg body mass of pickle juice, CHO-e drink, or tap water. Main Outcome Measure(s): Plasma sodium concentration, plasma magnesium concentration, plasma calcium concentration, plasma potassium concentration, plasma osmolality, and changes in plasma volume were analyzed. Urine specific gravity, osmolality, and volume were also measured to characterize hydration status. Results: Mean fluid intake was 86.3 ± 16.7 mL. Plasma sodium concentration, plasma magnesium concentration, plasma calcium concentration, plasma osmolality, and plasma volume did not change during the 60 minutes after ingestion of each fluid (P ≥ .05). Water ingestion slightly decreased plasma potassium concentration at 60 minutes (0.21 ± 0.14 mg/dL [0.21 ± 0.14 mmol/L]; P ≤ .05). Conclusions: At these volumes, ingestion of pickle juice and CHO-e drink did not cause substantial changes in plasma electrolyte concentrations, plasma osmolality, or plasma volume in rested, euhydrated men. Concern that ingesting these volumes of pickle juice might exacerbate an athlete's risk of dehydration-induced hypertonicity may be unwarranted. If EAMCs are caused by large electrolyte loss due to sweating, these volumes of pickle juice or CHO-e drink are unlikely to restore any deficit incurred by exercise.


1985 ◽  
Vol 248 (2) ◽  
pp. E155-E161
Author(s):  
S. W. Cheng ◽  
W. G. North

The responses of vasopressinergic neurons to acute salt loading and to graded hemorrhage were studied in rats under conscious and anesthetized conditions. Chronically cannulated rats were used in this study so that pre- and postanesthetic conditions could be studied in the same animals. Anesthesia induced by a combination of ketamine hydrochloride and pentobarbital sodium (Nembutal) did not cause a release of vasopressin-associated neurophysin (VP-RNP). In response to infusion of 18% saline, animals in the anesthetized state had significantly greater increases in plasma osmolality (Posmol) and plasma sodium concentration than animals in the conscious state. However, the rate of increase in plasma VP-RNP concentration ([VP-RNP]) as well as the relationship between [VP-RNP] and Posmol were not significantly different for the two states. Graded hemorrhage caused similar rates of increase in [VP-RNP] for animals under conscious and anesthetized conditions. These data suggest that anesthesia induced by ketamine plus pentobarbital sodium does not change the responsiveness of vasopressinergic neurons to acute salt loading and to graded hemorrhage.


2007 ◽  
Vol 293 (1) ◽  
pp. F333-F341 ◽  
Author(s):  
Chunling Li ◽  
Weidong Wang ◽  
Rikke Norregaard ◽  
Mark A. Knepper ◽  
Søren Nielsen ◽  
...  

The roles of epithelial sodium channel (ENaC) subunits (α, β, and γ) in the impaired renal reabsorption of sodium and water were examined in rat models with bilateral (BUO) or unilateral ureteral obstruction (UUO) for 24 h or with BUO followed by release of obstruction and 3 days of observation (BUO-3dR). In BUO rats, plasma osmolality was increased dramatically, whereas plasma sodium concentration was decreased. Immunoblotting revealed a significantly decreased expression of α-ENaC (57 ± 7%), β-ENaC (19 ± 5%), and γ-ENaC (51 ± 10%) as well as 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) in the cortex and outer medulla (C+OM) compared with sham-operated controls. This was confirmed by immunohistochemistry. BUO-3dR was associated with polyuria and impaired renal sodium handling. The protein abundance and the apical labeling of α-ENaC were significantly increased, whereas β- and γ-ENaC as well as 11β-HSD2 expression remained decreased. In UUO rats, expression of α- and β-ENaC and 11β-HSD2 decreased in the C+OM in the obstructed kidney. In contrast, the abundance and the apical labeling of α-ENaC in the nonobstructed kidneys were markedly increased, suggesting compensatory upregulation in this kidney. In conclusion, α-, β-, and γ-ENaC expression levels are downregulated in the obstructed kidney. The expression and apical labeling of α-ENaC were increased in BUO-3dR rats and in the nonobstructed kidneys from UUO rats. These results suggest that altered expression of α-, β-, and γ-ENaC may contribute to impaired renal sodium and water handling in response to ureteral obstruction.


1991 ◽  
Vol 261 (4) ◽  
pp. R1028-R1038 ◽  
Author(s):  
J. G. Verbalis ◽  
J. Dohanics

Neurohypophysial secretion of vasopressin (AVP) and oxytocin (OT) was studied in rats maintained under hyposmolar conditions for 10-24 days. Graded intravenous infusions of hypertonic saline solutions had no consistent effect on plasma AVP and OT levels until plasma sodium concentration ([Na+]) exceeded 130 mM, after which levels of both hormones increased as an exponential function of plasma [Na+]. Detectable increases in plasma AVP and OT began at significantly lower plasma [Na+] in hyposmolar rats than in normosmolar control rats (10.8 mM lower for AVP and 18.4 mM lower for OT). AVP and OT secretion in hyposmolar rats was also markedly blunted in response to nonosmotic stimuli, including acute and chronic hypovolemia and systemic administration of cholecystokinin. Cessation of 1-desamino-8-D-arginine vasopressin-induced antidiuresis resulted in an appropriately rapid correction of plasma [Na+] to normal levels within 24 h. Consequently, although chronic hyposmolarity caused a moderate downward resetting of the osmotic thresholds for AVP and OT secretion, it did not cause sustained deficits in osmoregulation. These results suggest that osmoreceptor activity is regulated to maintain extracellular fluid and plasma osmolality within narrow absolute ranges rather than responding to relative changes in osmolality.


2014 ◽  
pp. 83-89
Author(s):  
Dung Ngo ◽  
Thi Nhan Nguyen ◽  
Khanh Hoang

Objective: Study on 106 patients with closed head injury, assessment of serum ADH concentration, correlation with Glasgow score, sodium and plasma osmotic pressure. Patients and methods: Patients with closed head injuries were diagnosed determined by computerized tomography, admitted to the Hue Central Hospital 72 hours ago. Results: (i) Serum concentration of ADH 42.21 ± 47.80 pg/ml. (ii) There is a negative correlation between serum levels of ADH with: (1) Glasgow point r = -0.323, p <0.01; (2) Plasma sodium concentration r = - 0.211, p > 0.05; (3) Plasma osmotic pressure r = - 0.218, p> 0.05. Conclusion: There is a negative correlation between serum levels of ADH with Glasgow scale, plasma sodium concentration and osmotic pressure in plasma. Key words: ADH traumatic brain injury.


Nephron ◽  
2021 ◽  
pp. 1-3
Author(s):  
Rosa D. Wouda ◽  
Rik H.G. Olde Engberink ◽  
Eliane F.E. Wenstedt ◽  
Jetta J. Oppelaar ◽  
Liffert Vogt

1998 ◽  
Vol 275 (5) ◽  
pp. R1605-R1610 ◽  
Author(s):  
Takamasa Tsuchida ◽  
Yoshio Takei

The effects of eel atrial natriuretic peptide (ANP) on drinking were investigated in eels adapted to freshwater (FW) or seawater (SW) or in FW eels whose drinking was stimulated by a 2-ml hemorrhage. An intra-arterial infusion of ANP (0.3–3.0 pmol ⋅ kg−1 ⋅ min−1), which increased plasma ANP level 1.5- to 20-fold, inhibited drinking dose dependently in all groups of eels. The drinking rate recovered to the level before ANP infusion within 2 h after infusate was replaced by saline. The inhibition at 3.0 pmol ⋅ kg−1 ⋅ min−1was profound in FW eels and hemorrhaged FW eels, whereas significant drinking still remained after inhibition in SW eels. Plasma ANG II concentration also decreased dose dependently during ANP infusion and recovered to the initial level after saline infusion in all groups of eels. The decrease at 3.0 pmol ⋅ kg−1 ⋅ min−1was large in FW eels and hemorrhaged FW eels compared with that of SW eels. Thus the changes in drinking rate and plasma ANG II level were parallel during ANP infusion. Plasma sodium concentration and osmolality decreased during ANP infusion in SW and FW eels, and they were restored after saline infusion. In hemorrhaged FW eels, however, ANP infusion did not alter plasma sodium concentration and osmolality. Hematocrit did not change during ANP infusion in any group of eels. Collectively, ANP infusion at physiological doses decreased drinking rate and plasma ANG II concentration in parallel in both FW and SW eels. It remains undetermined whether the inhibition of drinking is caused by direct action of ANP or through inhibition of ANG II, which is known as a potent dipsogen in all vertebrate species, including eels.


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