Changes In Calcium Metabolism Research Articles

Prebiotics Enhance Magnesium Absorption and Inulin‐based Fibers Exert Chronic Effects on Calcium Utilization in a Postmenopausal Rodent Model

Age-related changes in calcium metabolism play a role in the development of osteoporosis. A 4-wk feeding study was conducted in 5-mo-old ovariectomized (OVX) Sprague-Dawley rats to assess the effect of various dietary fibers on mineral metabolism and bone health parameters. There were 6 treatment groups: sham-Control, OVX-Control, OVX rats receiving daily estradiol (E₂) injections, and OVX rats receiving an AIN-93M diet supplement with either an inulin-based fiber (Synergy1® or Fruitafit HD®) or a novel fiber (polydextrose) at 5% wt. of diet. Calcium and magnesium metabolic balances were performed after early (3 d) and late exposure (4 wk) to dietary treatments. Rats receiving polydextrose had significantly higher net calcium absorption efficiency and retention than all control groups and a trend (P≤ 0.10) for higher calcium absorption when compared to inulin-based fibers after early exposure but the advantage did not persist over long-term exposure. The inulin-based fibers had positive chronic effects on calcium metabolism that were related to changes in the gut, that is, production of short chain fatty acids and higher cecal wall weights. All fibers improved magnesium absorption and retention in early and late metabolic balances; effects on magnesium metabolism were more pronounced than for calcium. Steady growth in US middle-aged and elderly populations has led to higher incidences of several chronic diseases including osteoporosis, a bone disease that primarily affects postmenopausal women. Recent research suggests that certain dietary fibers (prebiotics) enhance mineral absorption and may impart bone health benefits. This work examines the impact of prebiotic supplementation on mineral metabolism and bone health using a postmenopausal rat model. Study findings will aid future investigations in ascertaining the factors related to potential bone health benefits of prebiotic which will aid in developing an effective prebiotics food product/supplement that will address the bone health needs of consumers.

Effects of dietary bread crust Maillard reaction products on calcium and bone metabolism in rats

Maillard reaction products (MRP) consumption has been related with the development of bone degenerative disorders, probably linked to changes in calcium metabolism. We aimed to investigate the effects of MRP intake from bread crust on calcium balance and its distribution, and bone metabolism. During 88 days, rats were fed control diet or diets containing bread crust as source of MRP, or its soluble high molecular weight, soluble low molecular weight or insoluble fractions (bread crust, HMW, LMW and insoluble diets, respectively). In the final week, a calcium balance was performed, then animals were sacrified and some organs removed to analyse calcium levels. A second balance was carried out throughout the experimental period to calculate global calcium retention. Biochemical parameters and bone metabolism markers were measured in serum or urine. Global calcium bioavailability was unmodified by consumption of bread crust or its isolate fractions, corroborating the previously described low affinity of MRP to bind calcium. Despite this, a higher calcium concentration was found in femur due to smaller bones having a lower relative density. The isolate consumption of the fractions altered some bone markers, reflecting a situation of increased bone resorption or higher turnover; this did not take place in the animals fed the bread crust diet. Thus, the bread crust intake does not affect negatively calcium bioavailability and bone metabolism.

Calcium metabolism and anti-aging of bone

Age-dependent change in calcium metabolism is affected by nutritional factors like calcium and vitamin D as well as by endocrine factors including parathyroid hormone. Because calcium deficiency could deteriorate bone metabolisms and cardiovascular systems, adequate intakes of calcium and vitamin D are important for anti-aging.

Disease-Modifying Mutations in Familial Hypertrophic Cardiomyopathy

Cardiomyopathies are primary disorders of cardiac muscle associated with abnormalities of cardiac wall thickness, chamber size, contraction, relaxation, conduction, and rhythm. They are a major cause of morbidity and mortality at all ages and, like acquired forms of cardiovascular disease, frequently progress into heart failure.1 In contrast to dilated cardiomyopathy (DCM), which is characterized by left or biventricular dilation in association with depressed myocardial contractility,1 familial hypertrophic cardiomyopathy (FHC) is characterized by increased cardiac mass with myocyte and myofibrillar disarray. The disease is associated with electrical instability (ie, atrial and ventricular arrhythmias), which makes it the leading cause of death in young athletes. There is marked diversity in the morphological features and clinical manifestations of both DCM and FHC.2 Article p 1820 Family studies have demonstrated that hypertrophic cardiomyopathy is a heritable disorder that is transmitted as an autosomal-dominant trait or as a sporadic disease. There is neither a racial nor an ethnic predisposition to this condition. Hypertrophic cardiomyopathy is not a rare condition; several noninvasive studies have demonstrated echocardiographic criteria for this disease in 0.2% of young adults (reviewed by Maron3). Genetic linkage studies in FHC have found disease loci on at least 14 different genes, most of them encoding sarcomeric genes; hence, FHC has been called a disease of the sarcomere. In addition, several mutations within the Ras pathway have been shown to cause at least syndromic forms of hypertrophic cardiomyopathy,4,5 pointing to the presence of additional but poorly understood disease-causing and/or modifier genes. Thus far, however, most of the clinical heterogeneity of FHC has been accounted for by the substantial diversity of gene defects that cause the condition (ie, up to 45% of disease-causing mutations have been observed in the β-myosin heavy chain [MHC] gene myh7 and up to 35% in …

Osteoporosis and halo traction in scoliosis patients (author's transl)

In 54 patients who underwent halo traction for an average of 80 days each, there was no laboratory evidence of any change in calcium metabolism. Histologically, there were slight but significant bony changes after termination of halo traction treatment, principally "low-turnover" osteoporosis, which was possibly more prevalent in female patients. Where a slight osteoporosis already existed prior to halo traction, it generally became more severe. The study seems to show that no relationship exists between the etiology of scolioses and the development of osteoporosis. It proves that in respect of the development of osteoporosis also, permanent halo traction is not a neutral procedure.

Management of Ventricular Arrhythmias in Heart Failure

Patients who have left ventricular dysfunction and heart failure are at high risk for ventricular tachyarrhythmias and sudden cardiac death. Re-entrant mechanisms around scar tissue, afterdepolarizations, and triggered activity due to changes in calcium metabolism significantly contribute to arrhythmogenesis. Amiodarone, class III antiarrhythmic agent, and beta-blockers are effective for control of ventricular arrrhythmias caused by heart failure and reduce sudden death as well as total mortality.

Cyclical Changes in Calcium Metabolism across the Menstrual Cycle in Women with Premenstrual Dysphoric Disorder

Alterations in calcium homeostasis have long been associated with affective disorders. Recently, it has been suggested that abnormalities in calcium metabolism may be responsible for some affective and somatic symptoms in women with premenstrual syndrome. Our objective was to measure fluctuations and group differences in calcium-regulating hormones across the menstrual cycle in women with and without premenstrual dysphoric disorder (PMDD). We conducted a cross-sectional and prospective study of women with and without PMDD. Participating women underwent 2 months of self-assessment symptom screening and 1 month of hormonal evaluation. Calcium-regulating hormones varied significantly across the menstrual cycle in both groups. Total serum, ionized and urine calcium, pH, intact PTH, and 1,25-dihydroxyvitamin D [1,25(OH)(2)D] varied significantly over the menstrual cycle. The PMDD group, when compared with controls, had significantly lower ionized calcium at phase 1 (menses) (1.166 +/- 0.072 vs. 1.182 +/- 0.087 mmol/liter; P = 0.027), significantly lower urine calcium excretion at three of the five phases (late follicular phase 2, midcycle phase 3, and early luteal phase 4), and significantly lower 1,25(OH)(2)D at luteal phase 4 (45.0 +/- 27.5 vs. 50.6 +/- 33.8 pg/ml; P = 0.032). Cyclical fluctuations of the calcium-regulating hormones may help us better understand some of the psychological and somatic features of PMDD. The lack of responsiveness in vitamin D metabolism resulting in a decline in 1,25(OH)(2)D during the luteal phase of the menstrual cycle may serve as the biological trigger for the classical features of PMDD.

Maternal plasma osteoprotegerin concentration in normal pregnancy

Pregnancy is associated with major changes in calcium metabolism because the neonatal skeleton contains approximately 30 g of calcium, which are largely deposited in the third trimester. Osteoprotegerin (OPG) acts as a decoy receptor for the "Receptor Activator of Nuclear Factor-kappaB Ligand" (RANKL), which is an essential factor for bone remodeling. This study was conducted to determine whether there were changes in maternal plasma OPG concentration during normal pregnancy. A cross-sectional study was performed in 433 patients of reproductive age (40 nonpregnant and 393 pregnant). Pregnant patients were classified into 4 groups according to gestational age: group 1: 11 to 14 weeks (n = 100); group 2: 15 to 18 weeks (n = 99); group 3: 27 to 30 weeks (n = 100); and group 4: 37 to 42 weeks (n = 94). Plasma OPG concentrations were measured with the use of a sensitive and specific immunoassay. Nonparametric statistics were used for analysis. OPG was detected in the plasma of all women tested. The median OPG concentration was significantly higher in term patients than in those in early pregnancy (median: 6.63 pmol/L [range: 1.57-25.57] vs median: 3.98 pmol/L [range: 0.41-13.71], P < .001). There was no significant difference in plasma OPG concentrations between nonpregnant women and those in groups 1 or 2 (nonpregnant women median: 3.86 pmol/L [range: 1.64-15.29] vs group 1 median: 3.98 pmol/L [range: 0.41-13.71] vs group 2 median: 3.87 pmol/L [range: 1.14-69.83], P = .75). The median maternal plasma OPG concentration is higher in the third trimester than in the first trimester of pregnancy. OPG may be involved in the regulation of bone turnover during pregnancy.

Vitamin D Receptor Fok1 Polymorphisms Affect Calcium Absorption, Kinetics, and Bone Mineralization Rates During Puberty

Few studies of the VDR polymorphisms have looked at calcium metabolism or long-term effects. We measured bone mineralization and calcium metabolic parameters longitudinally in a group of 99 adolescents. We found a significant relationship between calcium absorption and skeletal calcium accretion and the Fok1, but not other VDR or related, genetic polymorphisms. It seems that the Fok1 polymorphism directly affects bone mineralization during pubertal growth through an effect on calcium absorption. There are few data regarding the relationship between genetic markers for low bone mass and changes in calcium metabolism in childhood or adolescence. We sought to identify the effects of polymorphisms of the vitamin D receptor (VDR) on calcium and bone mineral metabolism in a longitudinal study of pubertal adolescents. Adolescents (n = 99) received comprehensive stable isotope studies of calcium absorption, bone calcium kinetics, and bone mineralization. Studies were repeated 12 months later. Polymorphisms of putative genetic markers were determined and related to bone mineralization and calcium metabolic finding. Results were analyzed by ANOVA in which changes over time were determined using the initial value as a covariate. Polymorphisms of the Fok1 gene of the VDR were significantly related to calcium absorption (p = 0.008) and whole body BMC (p = 0.03) and BMD (p = 0.006). The Fok1 effect on whole body BMD was significant for those with Ca intake >800 mg/day (p < 0.001), whereas for those with Ca intake < or = 800 mg/day, the Fok1 genotype did not have a significant effect on whole body BMD (p = 0.40). The Fok1 genotype was significantly related to the changes during the year in whole body calcium accretion, with the ff genotype having a 63 +/- 20 mg/day deficit compared with the FF genotype (p = 0.008). The Fok1 polymorphism of the VDR receptor seems to directly affect bone mineral accretion during pubertal growth through an effect on calcium absorption. The relationship between different genetic polymorphisms and bone mineral metabolism may vary by life stage as well as diet.

Maternal Calcium Intake and Metabolism During Pregnancy and Lactation

Calcium is an essential nutrient during pregnancy and lactation. Calcium contributes to bone development in the fetus and neonate and is considered a critical nutrient. Physiological changes in calcium metabolism occur during pregnancy and lactation. Some women may lose some of their bone density during pregnancy and/or lactation, and then regain it after the cessation of lactation. Implications for childbirth educators include content regarding the topic of calcium in their classes.

Interrelationship between bone turnover markers and dietary calcium intake in pregnant women: a longitudinal study

This longitudinal study evaluated bone turnover and the interrelationship between changes in bone biomarkers and habitual dietary calcium intake during pregnancy in a group of women ranging widely with regard to dietary calcium intake. Thirty-nine healthy pregnant and 30 nonpregnant women were studied. Calcium, phosphorus, 1α,25-dihydroxyvitamin D (1,25diHOD), bone alkaline phosphatase (bALP), carboxyterminal propeptides of type I procollagen (PICP) and carboxyterminal telopeptides of type I collagen (βCTX and ICTP) were measured in serum and calcium, and creatinine and aminoterminal telopeptide (NTX) were determined in urine. Serum calcium and phosphorus did not change but the urinary Ca/Creat ratio and 1,25diHOD increased throughout pregnancy (P < 0.001 and P < 0.0001, respectively). Serum b-ALP and PICP increased during the last two trimesters (P < 0.0001 and P < 0.001, respectively). All studied bone resorption markers increased compared to nonpregnant values throughout pregnancy. The highest increment was observed in the third trimester. The level of significance decreased as follows: βCTX > NTX >ICTP. Serum 1,25 diHOD versus calcium intake showed a positive and significant correlation (r = 0.51, P < 0.02). A negative correlation between the absolute change in βCTX, NTX, and b-ALP between the third and second trimester and calcium intake at the end of pregnancy was observed in pregnant women who did not cover adequately calcium intake requirements (r = −0.47, P < 0.03; r = −0.41, P < 0.05; and r = −0.43, P < 0.05, respectively). These results suggest that skeletal response to pregnancy may not be entirely independent of maternal calcium intake, especially in women with usually low calcium intake. In summary, not only hormonal changes in calcium metabolism that occur during pregnancy but also other considerations, such as low dietary calcium intake, may lead to an increment in the biological activity of the skeleton. Additional studies must be conducted to confirm our findings and to gain a better understanding of skeletal response to a low calcium intake during pregnancy.

Low Protein Intake: The Impact on Calcium and Bone Homeostasis in Humans

Increasing dietary protein results in an increase in urinary calcium. Despite over 80 y of research, the source of the additional urinary calcium remains unclear. Because most calcium balance studies found little effect of dietary protein on intestinal calcium absorption, it was assumed that the skeleton was the source of the calcium. The hypothesis was that the high endogenous acid load generated by a protein-rich diet would increase bone resorption and skeletal fracture. However, there are no definitive nutrition intervention studies that show a detrimental effect of a high protein diet on the skeleton and the hypothesis remains unproven. Recent studies from our laboratory demonstrate that dietary protein affects intestinal calcium absorption. We conducted a series of short-term nutrition intervention trials in healthy adults where dietary protein was adjusted to either low, medium or high. The highest protein diet resulted in hypercalciuria with no change in serum parathyroid hormone. Surprisingly, within 4 d, the low protein diet induced secondary hyperparathyroidism that persisted for 2 wk. The secondary hyperparathyroidism induced by the low protein diet was attributed to a reduction in intestinal calcium absorption (as assessed by dual stable calcium isotopes). The long-term consequences of these low protein-induced changes in calcium metabolism are not known, but they could be detrimental to skeletal health. Several recent epidemiological studies demonstrate reduced bone density and increased rates of bone loss in individuals habitually consuming low protein diets. Therefore, studies are needed to determine whether low protein intakes directly affect rates of bone resorption, bone formation or both.

Calcium Metabolism and a Mars Mission: New Problems

Results of ground-based and spaceflight experiments are analyzed using a mathematical model to predict long-term effects of the adaptation of human mineral metabolism that takes place during spaceflights of extended duration. The changes in calcium metabolism induced by spaceflight, both real and simulated, are summarized. These changes include a decline in the amount of calcium in the bone pool inexchangeable with free calcium and a decrease in the capacity of tissue and blood buffer systems to retain calcium. In the mathematical model of calcium metabolism, the rates of the main calcium fluxes were estimated for normal conditions and for stress conditions mimicking the 110th day of spaceflight according to the rate of calcium efflux from bone. This analysis showed that, under ordinary living conditions, a 1-h calcium load of 8 mmol/h would give rise to only a 20% transient increase in PCa++, causing a 17-fold increase in the calcium binding by tissue and blood buffer systems and an 11-fold increase in binding of the ion by blood buffers. The calcium content in woven bone was predicted to increase by 10–11% in response to this calcium load. The activity of the regulatory mechanisms in the model was varied. When the blood level of the active metabolite of vitamin D3 was set to one-tenth of its norm, the rate of compact bone resorption changed only slightly. As calculated in the model, the calcium input from woven bone can be normalized by raising the calcitonin level 20-fold or by completely blocking the secretion of parathyroid hormone, neither of which is realistically achievable, whether on land in experiments simulating weightlessness or during spaceflight. The results of experiments and the data of simulation using the model show that none of the active calcium regulators tested can offset a microgravity-induced decline in the ability of calcium stores to retain calcium.

Calcium homeostasis and intact plasma parathyroid hormone during exercise and training in young Standardbred horses.

Physical exercise is known to affect calcium homeostasis in horses, but there is little information on the hormonal regulation of calcium metabolism during exercise. In order to evaluate the effects of exercise and training on calcium homeostasis and intact plasma parathyroid hormone, 7 untrained Standardbred horses were studied in a 6 week training programme. These horses were accustomed to running on the treadmill 3 weeks before onset of training and were exercised on a high-speed treadmill with an initial incremental standardised exercise test (SET 1: 6 incremental steps of 5 min duration each; first step 5 m/s, increase 1 m/s). SET 1 was followed by a lactate-guided training programme (6 weeks in total) with 2 types of exercise in alternating order with a day of rest after each work day: high-speed exercise (HSE) of 15 min duration, starting at VLa4, continuous increase in speed every 60 s by 0.3 m/s (14 incremental steps); and low-speed exercise (LSE) at a constant velocity at VLa2.5, duration approximately 60-90 min. The whole training programme consisted of 8 HSE and 8 LSE sessions. HSE and LSE were calculated to require the same energy expenditure. A final SET (SET 2) finished the training programme. Blood samples for lactate, plasma total calcium [Ca], blood ionised calcium [Ca2+], blood pH, plasma inorganic phosphorus [P(i)] and plasma intact parathyroid hormone [PTH] were collected before, during and after SETs 1 and 2, before and after the first and eighth HSE and LSE. During SETs 1 and 2, HSEs 1 and 8 there was a decrease in ionised Ca2+ and pH and a rise in lactate, intact PTH and P(i). LSEs 1 and 8 resulted in an increase in pH, whereas lactate, ionised Ca2+, total Ca, P(i) and intact PTH were not affected. No changes in calcium metabolism were detected during training. Results of this study suggest that intact PTH is a mediator in counter-regulation of exercise-induced hypocalcaemia.

Calcium requirement for the maintenance of bone mass

The bone mineral density of middle-aged and elderly people is determined by the peak bone mass obtained in the adolescent period and the bone loss in the later stage of life. The rapid bone loss observed in the postmenopausal women is largely explained by estrogen deficiency. On the other hand, aging-dependent decrease of bone mass commonly seen in women and men may be attributed to the change in calcium metabolism. In Japan, the calcium intake would be less than the amount sufficient to keep positive calcium balance and to maintain bone mass.

Synergistic Activation of NFAT by HIV-1 Nef and the Ras/MAPK Pathway

Nef is a lentiviral protein involved in pathogenesis of AIDS, but its molecular mechanisms of action remain incompletely understood. Here we report a novel effect of Nef on lymphocyte signaling, which is mediated via a T cell receptor (TCR)-independent contribution of Nef to induction of nuclear factor of activated T cells (NFAT), a transcription factor that plays a central role in coordinating T cell activation. Expression of Nef did not significantly alter the basal level of NFAT activity in Jurkat cells nor the increased activity following T cell receptor stimulation by anti-CD3 or anti-CD3 + anti-CD28. We also mimicked NFAT induction by TCR triggering by simultaneous activation of the Ras and calcium signaling pathways with phorbol 12-myristate 13-acetate and ionomycin, respectively. Strikingly, whereas activation of either of these pathways individually did not induce NFAT activity in control cells, in Nef-expressing cells phorbol 12-myristate 13-acetate treatment alone resulted in a 100-fold increase in NFAT-directed gene expression. Experiments with different dominant negative mutant signaling proteins, inhibitory chemicals, and Lck-deficient Jurkat cells revealed that this effect was mediated via activation of calcineurin by Nef-induced changes in calcium metabolism, but was independent of TCR-associated signaling events. This ability of Nef to substitute for triggering of the calcium pathway in induction of NFAT could promote activation of human immunodeficiency virus (HIV)-infected T cells in response to stimuli mediated via TCR or other cell surface receptors under conditions when activation of Ras rather than calcium signaling would otherwise predominate.

Arrhythmias in heart failure: current concepts of mechanisms and therapy.

About one half of deaths in patients with heart failure are sudden, mostly due to ventricular tachycardia (VT) degenerating to ventricular fibrillation or immediate ventricular fibrillation. In severe heart failure, sudden cardiac death also may occur due to bradyarrhythmias. Other dysrhythmias complicating heart failure include atrial and ventricular extrasystoles, atrial fibrillation (AF), and sustained and nonsustained ventricular tachyarrhythmias. The exact mechanism of the increased vulnerability to arrhythmias is not known. Depending on the etiology of heart failure, different preconditions, including ischemia or structural alterations such as fibrosis or myocardial scarring, may be prominent. Reentrant mechanisms around scar tissue, afterdepolarizations, and triggered activity due to changes in calcium metabolism significantly contribute to arrhythmogenesis. Furthermore, alterations in potassium currents leading to action potential prolongation and an increase in dispersion of repolarization play a significant role. Treatment of arrhythmias is necessary either because patients are symptomatic or to reduce the risk for sudden cardiac death. The individual history, left ventricular function, electrophysiologic testing, and the signal-averaged ECG give useful information for identifying patients at risk for sudden cardiac death. The implantable cardioverter defibrillator (ICD) has evolved as a promising therapy for life-threatening arrhythmias. A potential role may exist for antiarrhythmic drugs, mainly amiodarone. There is growing evidence that patients with sustained VT or a history of resuscitation have the best outcome with ICD therapy regardless of the degree of heart failure. Many of these patients require additional antiarrhythmic therapy because of AF or nonsustained VTs that may activate the device. Catheter ablation or map-guided endocardial resection are additional options in selected patients but seldom represent the only therapeutic strategy.

Effect of increasing age on diastolic motion of the left ventricular atrioventricular plane in normal subjects

Aims: To determine the effect of ageing on diastolic motion of the atrioventricular plane in normal subjects. Methods and results: One hundred normal subjects (age range 43 to 78 years) underwent an echocardiographic examination and determination of diastolic motion of the atrioventricular plane. The total displacement declined with increasing age at the septum ( p<0.01) but not at other sites. The rate of change of early displacement declined with increasing age at all sites ( p<0.001). The displacement due to atrial systole increased with increasing age ( p<0.05). Conclusion: Important changes in diastolic function in normal subjects occur in the fifth and sixth decades. This may relate to the change in calcium metabolism within the myocardium seen with increasing age. It is not possible to determine from the study whether these changes are due to ageing per se or to environmental factors associated with ageing.

Use of Calcium Tracers and Biomarkers to Determine Calcium Kinetics and Bone Turnover

The purpose of this article is to review approaches to measuring calcium metabolism and bone turnover, which can be used to assess bone loss during spaceflight and to evaluate the effectiveness of interventions aimed at reducing bone loss. Isotopic tracers of calcium can be used to determine absorption, excretion, retention, body pool sizes, and turnover rates. Because 99% of the body’s calcium is in the bone, calcium tracer kinetics can provide an accurate assessment of bone turnover rates. Biomarkers can be used to assess qualitative changes in bone formation and bone resorption, but they do not predict bone density or quantitate net calcium retention. The usefulness of biomarkers has been validated against calcium tracer kinetics and bone histomorphometry. Calcium kinetics and biomarkers of bone turnover can assess changes in calcium metabolism and bone turnover long before changes in bone density can be detected.

Calcium metabolism and osmoregulation during sexual maturation of river running Atlantic salmon

As Atlantic salmon return from the ocean to undertake the anadromous spawning migration up the river of origin, profound changes in calcium metabolism and osmoregulation take place. Using tartrate resistant acid phosphatase as a marker, scale osteoclast activity was found to increase throughout sexual maturation and spawning migration. Thus, the participation of osteoclasts in the elevated scale resorption observed during this phase is established. As calcium was simultaneously accumulated in the female gonads, it is proposed that the scales are resorbed in order to provide calcium for the growing ovaries. Plasma oestradiol‐17β levels were elevated in females during sexual maturation, and had decreased at the time of spawning. Plasma testosterone levels were similar in males and females during the first part of the upriver migration, but had increased in males and decreased in females at spawning. In addition to the role of these sex steroids in the gonadal growth, their possible involvement in the increased scale resorption during this phase is discussed. Plasma growth hormone and thyroxine levels were elevated in both sexes at spawning, with the triiodothyronine/thyroxine (T3/T4) ratio declining sharply, indicating possible roles for these hormones in the maturational process. The relatively low gill Na+, K+‐ATPase activity of salmon caught in the estuary implies that the fish had already adapted to a hypoosmotic environment. During the upriver migration, the gill Na+, K+‐ATPase activity decreased further, indicating that the hypoosmoregulatory ability was suppressed further during sexual maturation and spawning migration.