Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.6.1.3 (ATPase)
65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied papillary muscle mechanics and energetics, myosin phenotype, and ATPase activities in left ventricles from rats bearing a growth hormone (GH)--secreting tumor. 18 wk after tumor induction, animals exhibited a dramatic increase in body weight (+101% vs. controls) but no change in the ventricular weight/body weight ratio. The maximum isometric force of papillary muscles normalized per cross-sectional area rose markedly (+42%, P less than 0.05 vs. controls), whereas the maximum unloaded shortening velocity did not change. This was observed despite a marked isomyosin shift towards V3 (32 +/- 5% vs. 8 +/- 2% in controls, P less than 0.001). Increased curvature of the force-velocity relationship (+64%, P less than 0.05 vs. controls) indicated that the muscles contracted more economically, suggesting the involvement of V3 myosin. Total calcium- and actin-activated myosin ATPase activities assayed on quickly frozen left ventricular sections were similar in tumor-bearing rats and in controls. After alkaline preincubation, these activities only decreased in tumor-bearing rats, demonstrating that V3 enzymatic sites were involved in total ATPase activity. These data demonstrate that chronic GH hypersecretion in the rat leads to a unique pattern of myocardial adaptation which allows the muscle to improve its contractile performance and economy simultaneously, thanks to myosin phenoconversion and an increase in the number of active enzymatic sites.
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PMID:Effects of chronic growth hormone hypersecretion on intrinsic contractility, energetics, isomyosin pattern, and myosin adenosine triphosphatase activity of rat left ventricle. 214 10

The cardiac effects of excess growth hormone (GH) were studied in the intact adult rat and in tissues prepared from the rat. Female Wistar-Furth rats were inoculated with a clonal cell line of pituitary cells which secrete GH. Five weeks later, heart weight had increased 37% compared to control (P less than 0.01) due to concomitant increases in left and right ventricular weight. Hemodynamic measurements in the anesthetized rat showed that GH stimulated rats had a decrease in blood pressure and heart rate and a small increase of left ventricular end-diastolic pressure (P less than 0.05). Measurement of left ventricular contractility and relaxation, and response to beta-adrenergic stimulation were decreased in GH compared to control (P less than 0.05). Contractile protein biochemistry showed an 18% reduction in Ca2(+)-myosin ATPase activity of the left ventricle (P less than 0.05) and non-denaturing pyrophosphate gels of purified myosin demonstrated a significant shift of isoforms from the exclusive V1 pattern to both V1 and V3 isomyosins in both ventricles (P less than 0.05). In contrast to the physiological and protein biochemistry adaptations, left ventricular morphology by light microscopy and ultrastructure by electron microscopy were normal in the GH stimulated heart. There were no significant changes in myofibril fraction, in the myofibril to mitochondria ratio or in the capillary numerical density of the hypertrophied left ventricle (P = N.S.). This study demonstrates that under prolonged and extreme stimulation by GH, the heart undergoes considerable growth/hypertrophy. Although cardiac morphology remains normal during this growth, there are alterations of the isomyosins such that ATPase activity is diminished and ventricular function is decreased.
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PMID:Cardiac physiology, biochemistry and morphology in response to excess growth hormone in the rat. 214 88

The role of growth hormone (GH) and cortisol in the development of hypoosmoregulatory mechanisms in sea trout parr, Salmo trutta trutta, was investigated by injecting freshwater (FW) yearlings every second day with saline, ovine growth hormone (oGH, 2.0 micrograms/g), cortisol (hydrocortisone hemisuccinate, 8.0 micrograms/g), or oGH + cortisol for a maximum of 14 days. Subgroups of the treated fish were transferred to three-fourths seawater (SW) after 7 or 15 days of treatment and the effects on plasma Na+, Cl-, muscle water content, gill Na+/K(+)-ATPase activity, and gill interlamellar chloride cell density were examined. In FW, gill Na+/K(+)-ATPase chloride cell density, and chloride cell apical to basal length increased by all hormone treatments, most significant by oGH + cortisol treatment. Plasma ions and muscle water content were unaffected in FW. Both SW transfers resulted in considerable mortality (50%) in control fish, whereas few cortisol-treated and no GH-treated or GH + cortisol-treated fish died. Plasma Na+ and Cl- levels increased dramatically (greater than 50%) in control fish and muscle water content decreased (8%) on Day 2 after both transfers. All hormone-treated groups regulated plasma ions and muscle water significantly better than controls in SW, indicating the physiological significance of the treatment. Notably, the oGH + cortisol-treated fish showed only insignificant changes in ion-osmotic homeostasis after SW transfer, suggesting a synergistic effect of the two hormones. It is concluded that treatment with the two hormones increases the salinity tolerance of sea trout parr at a developmental stage where FW life is obligatory.
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PMID:The role of cortisol and growth hormone in seawater adaptation and development of hypoosmoregulatory mechanisms in sea trout parr (Salmo trutta trutta). 216 6

Endogenous factors cross-reacting with antidigoxin antibodies have been found in several tissues and body fluids of animals and humans, using commercially available digoxin radioimmunoassay or enzyme immunoassay methods. The chemical characteristics of these endogenous factors are, at present, unknown, although it has been suggested that they could be substances with low molecular weight. Experimental studies and theoretical considerations indicate that endogenous digitalis-like factors (DDLFs), in addition to the ability to react with antibodies, might also bind to the specific cellular receptor of the cardiac glycosides and thus inhibit the membrane Na+/K(+)-ATPase (sodium pump). Therefore, EDLF can be an endogenous modulator of the membrane sodium-potassium pump and several authors have suggested that EDLF could play a role in the regulation of fluids and electrolytes, muscular tone of myocardial and also in the pathogenesis of arterial hypertension. In this review, the authors discuss the hypothesis that, in metabolic diseases such as diabetes mellitus, obesity and acromegaly, the sodium retention and volume expansion, possibly due to exaggerated sodium intake, and/or exogenously induced peripheral hyperinsulinemia and high levels of growth hormone, could trigger a sustained release of EDLF, which in turn increases the blood pressure.
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PMID:Is the endogenous digitalis-like factor the link between hypertension and metabolic disorders as diabetes mellitus, obesity and acromegaly? 222 23

Fischer 344 rats at various ages throughout the life span have been treated with growth hormone, clonidine, and insulin-like growth factor-I to restore circulating somatomedin levels in old animals to levels found in younger rats. The injections were intended to reverse (2-week treatments) or prevent (6-month treatments) deleterious effects of aging on skeletal muscle--specifically the loss of fast fibers during the latter part of the life span. However, measurements of myosin ATPase (and subsequent histochemical fiber type determinations) revealed that the previously reported age-related decrease in ATPase activities and fast fiber content did not occur in barrier-protected specific pathogen free rats or mice. None of the treatments used had a significant effect on the ATPase activity or fiber composition of soleus, extensor digitorum longus, or diaphragm muscles, although parallel determinations in collaborating laboratories verified that the hormones had major effects in other systems. Previously reported decreases with age in ATPase activity of heart muscle were confirmed in our experiments, and these decreases were shown to reflect a change in myosin isozyme composition of the hearts, both at the protein and the mRNA levels of gene expression.
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PMID:Skeletal muscle fiber types and myosin ATPase activity do not change with age or growth hormone administration. 252 6

To obtain more information on the role of prolactin and growth hormone during the parr-smolt transformation of Atlantic salmon, a population of fish in fresh water was sampled from January to June during two consecutive years. Gill Na+,K+-ATPase activity increased steadily during smoltification and a plasma thyroxine peak was observed 2-3 weeks before the gill Na+,K+-ATPase peak. On the basis of these two parameters, smoltification was considered complete in our populations in April 1985 and May 1986. Two peaks in plasma growth hormone levels occurred in 1986, one in mid-April and the second in mid-May. In both cases, these peaks coincided with a peak in plasma triiodothyronine and preceded the thyroxine peak by 1-2 weeks. Moreover, the second peak which lasted for 1 month coincided with maximal gill Na+,K+-ATPase activity. A decrease in plasma prolactin levels was observed during smoltification of Atlantic salmon in 2 consecutive years. During this period of decreasing and low plasma prolactin levels, gill Na+,K+-ATPase activity increased to its highest values. Atlantic salmon smolts were also directly transferred into seawater. After 2 days or more in seawater, plasma prolactin levels were not significantly different from those on Day 0, whereas in fresh water they showed large fluctuations. All these data indicate that growth hormone may play an important role in the development of hypoosmoregulatory activity. Increased hypoosmoregulatory ability also appears to be associated with low prolactin levels.
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PMID:Smoltification and seawater adaptation in Atlantic salmon (Salmo salar): plasma prolactin, growth hormone, and thyroid hormones. 254 14

This study investigates the effects of hypophysectomy and subsequent hormone replacement therapy upon the hormonal and osmoregulatory status of coho salmon, Oncorhynchus kisutch, in 7% seawater (SW) and SW. Following hypophysectomy, coho salmon were injected every 2 days for 8 days with thyroxine, growth hormone, and cortisol, alone or in combinations, and sampled 2 days after the final injection. Increased environmental salinity raises plasma sodium, calcium, and magnesium levels, as well as plasma osmolality. Cortisol is hypercalcemic and thyroxine is hypocalcemic in hypophysectomized salmon, but it is unclear whether these effects are due directly to calcium regulation or are the consequence of general effects on the plasma osmotic/ionic balance. Growth hormone and thyroxine together, but not separately, decrease and increase magnesium levels, at low and high environmental salinities, respectively, indicating a complex endocrine control of plasma magnesium. Gill Na+, K+-ATPase activity in hypophysectomized salmon is stimulated by growth hormone and cortisol, but inhibited by thyroxine and raised environmental salinity. This implies a complex endocrine control and indicates that hormonal support is needed to sustain or raise gill Na+, K+-ATPase activity in seawater. Increased environmental salinity induces elevation of plasma cortisol levels in apparent absence of pituitary control, indicating that the interrenals may respond to changes in external and/or internal environment, either directly or indirectly through extrapituitary hormonal or nervous control. Cortisol is a potent inhibitor of calcitonin secretion, as seen by the large decrease in plasma calcitonin levels in cortisol-treated hypophysectomized fish. The study was carried out at a time when thyroxine plasma levels were low. These basal levels were not affected by hypophysectomy, possibly indicating a basal release of thyroxine from the thyroid without stimulatory support of the pituitary gland.
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PMID:Effects of hypophysectomy and subsequent hormonal replacement therapy on hormonal and osmoregulatory status of coho salmon, Oncorhynchus kisutch. 283 Jan 61

In a study of the hormonal control of salmon smoltification, L-thyroxine (T4; 200 ppm in diet), ovine growth hormone (oGH; 2 micrograms/g intramuscular injection weekly), or a combination of these hormones was administered to underyearling amago salmon parr for 72 days. Administration of both T4 + oGH remarkably stimulated growth of the fish. All hormone treatments caused body silvering of the fish. The body silvering was the greatest in the group treated with T4 + oGH. Both T4 + oGH and oGH increased survival rate of the fish in 32% seawater, and kept plasma osmolarity and plasma sodium concentration lower than those of T4-treated and control groups in 27% seawater. Significant elevation of gill Na+, K+-ATPase activity was found in T4 + oGH-treated fish. On the other hand, T4 by itself did not affect the seawater tolerance of the fish. These findings suggest that GH or synergistic action of GH and T4 plays an important role in seawater adaptation during smoltification of amago salmon.
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PMID:Effects of L-thyroxine and ovine growth hormone on smoltification of amago salmon (Oncorhynchus rhodurus). 298 81

Salmonid species which undergo smoltification show a concurrent enhancement in saltwater (SW) osmoregulatory ability. This developmental change is marked by an increase in SW tolerance and gill Na+,K+-ATPase activity which appears to result, in part, from an increase in gill chloride cell density. Previous studies have suggested that cortisol and growth hormone (GH) may stimulate SW osmoregulatory mechanisms in salmonids. In this study, these hormones were examined for their ability to induce smoltification-associated osmoregulatory changes in pre- and desmoltified coho salmon (Oncorhynchus kisutch). Cortisol treatment for 12 days increased gill Na+,K+-ATPase activity in presmolts and gill residual (Na+,K+-independent) ATPase activity in both groups. Chloride cell density in presmolt primary and secondary lamellae and in desmolt secondary lamellae was increased as well. The rise in plasma sodium levels in fish transferred to SW was reduced only in desmolts. Treatment with bovine GH for 12-13 days increased gill Na+,K+-ATPase activity in presmolts and in desmolts. However, GH treatment in either group did not increase gill residual ATPase activity or alter plasma sodium levels in SW-transferred animals. Gill chloride cell density in presmolts also was unaffected (desmolts were not examined). Thus, both cortisol and GH are partially able to produce changes similar to those observed during smoltification. The contrasting effects of these hormones on gill chloride cell density and gill residual ATPase activity suggest that cortisol may stimulate chloride cell proliferation and/or differentiation, whereas GH may act specifically to increase gill Na+,K+-ATPase activity.
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PMID:Effects of cortisol and growth hormone on osmoregulation in pre- and desmoltified coho salmon (Oncorhynchus kisutch). 302 4

Beta-adrenoceptor stimulation in vivo shifts potassium into the cells. To examine whether human erythrocytes participate in this process, we measured, along with serum or plasma potassium, the concentrations of potassium and sodium in erythrocytes. Beta-adrenoceptor stimulation was obtained by infusion of either fenoterol or hexoprenaline into 6 volunteers at rest or by endogenous amines provoked in 14 volunteers during ergometric exercise. Metabolic effects were followed at rest on serum insulin, C-peptide, and growth hormone levels, and during exercise on pH on lactate concentration in blood. The potassium concentration (mean +/- S.E.M.) dropped (p less than 0.01) in serum from 4.64 +/- 0.37 to 3.19 +/- 0.43 mmol x l-1 in the first hour at rest and in plasma from 5.70 +/- 0.93 to 4.63 +/- 0.45 in 90 sec directly after exercise. The concentration of erythrocyte sodium dropped (p less than 0.001) from 9.68 +/- 0.73 to 8.81 +/- 0.62 mmol x l-1 in cells and from 9.62 +/- 1.16 to 8.55 +/- 1.24 during exercise for 90 s, respectively. Changes in the concentration ratio of cellular sodium to potassium confirmed this sodium shift. An increased sodium transport in erythrocytes due to beta-adrenoceptor stimulation in vivo appears to complement a shift of serum potassium into the cells and may be mediated by the membrane-bound sodium, potassium ATPase.
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PMID:Activation of sodium transport in human erythrocytes by beta-adrenoceptor stimulation in vivo. 304 Mar 90


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