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 have demonstrated previously that a variety of agents including corticosteroids, thyroid hormone, cationophores, methylxanthines, and analogues of cAMP--all of which have diversified functions in various tissues--elevate cellular angiotensin converting enzyme (ACE) activity of bovine endothelial cells in culture. In addition to these agents, we have now found that direct and receptor-mediated stimulators of adenylate cyclase, i.e., forskolin and cholera toxin, increase cellular ACE activity after 48 h incubation in culture. In an attempt to search out a more unifying concept of these stimulatory effects, we have further investigated the roles of second messengers in the stimulatory actions. Ca2+ ionophore A23187 produced significant increases in both intracellular Ca2+ and ACE of endothelial cells. In contrast to Ca2+ ionophore, agents that transiently mobilize Ca2+ from intracellular reserves such as bradykinin, acetylcholine, and ATP have no effect on the level of cellular ACE. Representative agents that elevate cellular cAMP (e.g., isobutyl methylxanthine [IBMX] and dibutyryl cAMP) elevated cellular ACE, but the slightly increased [Ca2+]i produced by these agents did not reach statistical significance. While IBMX, cholera toxin, and forskolin elevated cellular cAMP, other ACE stimulatory agents (hormones and cationophores) had no effect on cAMP. Ca2+ ionophore and the agents that elevated intracellular cAMP potentiated the effect of dexamethasone, thyroid hormone, and aldosterone in elevating cellular ACE activity. Increases in ACE activity produced by all stimulants were inhibited by the presence of 10-50 nM ouabain in the culture medium. Inhibition of ACE elevation by oubain was reversed by increasing the extracellular [K+], thereby implicating Na+, K(+)-ATPase in the ACE regulatory mechanism. These results support the presence of multiple independent mechanisms for the regulation of cellular ACE. In addition to possible involvement of intracellular Ca(2+)- and cAMP-dependent pathways, ACE is also increased by corticosteroids and thyroid hormone through mechanisms unrelated to Ca2+ and cAMP.
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PMID:Involvement of second messenger systems in stimulation of angiotensin converting enzyme of bovine endothelial cells. 165 91

A study was made of effects of aldosterone, aldosterone+dexamethasone, and aldosterone+spironolactone on Na,K-ATPase mRNA expression in renal cortex of adult and 10 day old rats, when kidney is not sensitive to the hormone injection. It is shown that hormonal induction of synthesis of Na,K-pump mRNA occurs in the early postnatal period apart from mineral corticoid receptors. It seems probable that aldosterone exerts its action in 10 day old rats by interaction with glucocorticoid receptors inducing synthesis of different amounts of alpha- and beta-subunits of Na,K-ATPase.
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PMID:[The hormonal regulation of mRNA Na,K-ATPase expression in rat kidneys in postnatal ontogeny]. 166 47

Natriuretic hormone is a digoxin-like substance that inhibits Na-K-ATPase, membraneous sodium pump, leads to storage of sodium in the cells, increases their tone which plays a key role in the increase of peripheral resistance of the blood vessels and progression of hypertensive disease. Results indicate that the level of natriuretic hormone was increased at all stages of hypertensive disease, positively correlated with aldosterone and kallikrein and negatively--with the plasma renin activity that confirms its pressor action.
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PMID:[The role of the natriuretic hormone in neurohumoral regulation in hypertension]. 168 83

The effects of aldosterone on protein synthesis in the latent period were investigated on cultured renal collecting duct cells from neonatal rabbit kidneys. Tissue was incubated with radioactively labelled uridine and amino acids and then precipitated with trichloroacetic acid in order to determine the intracellular precursor pool and identify new synthesis of RNA and protein. During the latent period, aldosterone increased the intracellular radioactive uridine pool and total radioactive RNA content already 20 and 60 min after its application; conversely 40 min after aldosterone introduction, no stimulation was found. Further experiments revealed that the intracellular radioactive amino acid pool was generally increased by aldosterone after 20, 40 and 60 min, while a distinct increased radioactive protein content was found to be induced by aldosterone only after 40 min. This indicates that aldosterone increases the uptake of RNA and protein precursors and the new synthesis of RNA and proteins. These events seem to to be regulated not continuously but intermittently. The induced proteins possibly take part in the mediation of the early hormone response. Experiments with the aldosterone antagonist, spironolactone, provide evidence for the specificity of the described hormone effects. The results after application of the Na+ channel blocker, amiloride, and the Na+/K(+)-ATPase inhibitor, G-strophanthin, indicate that the aldosterone effects are controlled by Na+ channels and Na+ pumps and therefore by the intracellular Na+ content. The inhibitory effect of cycloheximide on the aldosterone-induced protein synthesis indicates the role of these proteins on the hormone-stimulated Na+ transport.
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PMID:Action of aldosterone on cultured renal collecting duct cells during the latent period. 170 11

For several years now, it has been known that the administering of adrenergic beta antagonists, especially of the beta-2 type, induce hypokalemia as a result of the entering of potassium into the skeletal muscle cells. This fall in kalemia occurs independently from the effect of insulin, aldosterone or kidney excretion, is mediated by the beta-2 receptors and require the intervention of cAMP joined at the cell membrane and the subsequent stimulation of the Na-K-ATPase which bring the potassium into the striated muscle cell. Among the most outstanding drugs with beta-2 effect is salbutamol, which maintains the hypokalemic effect whether administered intravenously or inhaled. It has been used in cases of hyperkalemia, in both children and adults. The initially used intravenous dosage (0.5 mg) caused several side-effects, especially rapid heart beat, seen more in children. It has been recently found that the use of doses as low as 4 micrograms/kg lower the kalemia to values averaging 1.4 to 1.6 mEq/L (mmol/L); in addition, using these dosages intravenously in an average of 20 minutes, no side-effects were seen, even when administered to newborns. For the above, we considered that salbutamol, in the suggested dosages, constitutes an efficient and secure therapeutic method for the initial treatment of severe hyperkalemic patients.
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PMID:[The treatment of hyperkalemia with salbutamol]. 176 53

Methods for quantitative extraction and enrichment of digoxin-like immunoreactive substances (DLIS) from human cord blood plasma (CBP) using organic solvents combined with a solid state absorbent are presented. Sephadex LH-20 column chromatography is more suitable than sephadex G-25 for DLIS separation and purification from CBP extract. The elution pattern of sephadex LH-20 chromatography of deproteinized and desalted CBP shows two distinct DLIS peaks. The first peak coelutes with the steroids aldosterone, cortisol, progesterone, 17-OH-progesterone, testosterone and estradiol, while the second DLIS peak coelutes with dehydroepiandrosterone sulfate (DHEA-S). The Na+,K(+)-ATPase inhibitory activity peak partially overlaps with the first DLIS peak. Coeluted steroids could account only partially for digoxin-like immunoreactivity in the first DLIS peak; however, they did not contribute to the Na+,K(+)-ATPase inhibitory activity, whereas the second DLIS peak could be ascribed to endogenous DHEA-S.
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PMID:Digoxin-like immunoreactivity in cord blood plasma extracts is not only due to endogenous corticosteroids. 177 87

Modern biology provides satisfactory explanations for the abnormalities of the different phases of relaxation and diastole. Ventricular filling depends on three factors: active relaxation; the only factor is the concentration of ATP which has to re-increase. This requires elimination of the cytoplasmic calcium which activates ATP-ase by the Ca2+ ATPase of the sarcoplasmic reticulum and the Na+/Ca2+ pump. In hypertrophy, the concentration of the first and the activity of the second are decreased; passive wall compliance, which depends on the quantity and quality of parietal collagen. This factor is partially regulated in the myocardium by the concentration of aldosterone and angiotensin II; atrial contraction, which depends on the size of the atria and their isomyosine content. This changes in atrial overload to a slow form of myosine, one of the mechanisms of adaptation.
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PMID:[Biologist's view on diastolic dysfunction]. 183 66

Two types of proton-translocating ATPases, H-ATPase and H-K-ATPase, are found in the renal tubular cells. H-ATPase is present in both endocytic vesicles and apical membranes in almost all nephron segments. On the other hand, H-K-ATPase is present only in the connecting tubule and collecting duct. There is evidence to suggest that H-ATPase may be involved in H secretion in almost all nephron segments. H-K-ATPase is involved not only in H secretion but also in K absorption in the collecting duct segments. Aldosterone administration and metabolic acidosis stimulate the activity of H-ATPase in all collecting duct segments, whereas hypokalemia has only a limited effect on H-ATPase activity. On the other hand, hypokalemia, as well as metabolic acidosis, stimulates H-K-ATPase activity in the collecting duct segments, whereas aldosterone administration alone plays a minor role in the regulation of this enzyme. The physiological role and regulation of H-ATPase in the proximal tubule has not been established.
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PMID:Respective roles of H-ATPase and H-K-ATPase in ion transport in the kidney. 183 66

To characterize renal transport of Na+ in heart failure, urinary Na+ excretion (UNaV), aldosterone levels, and Na,K-ATPase activity in isolated nephron segments were determined in three groups: control rats, rats with heart failure and moderate sodium retention, and rats with heart failure and severe sodium retention. Heart failure was induced by a fistula between the aorta and vena cava. For the control group, UNaV was 0.66 +/- 0.04 (mean +/- SEM) mueq/min, and aldosterone was 18.4 +/- 3.5 ng%. Na,K-ATPase activity (in 10(-11) mol/mm/min) was 28.4 +/- 1.1 in the proximal convoluted tubule, 23.3 +/- 1.0 in the proximal straight tubule, 37.4 +/- 1.9 in the medullary thick ascending limb, 40.2 +/- 1.9 in the cortical thick ascending limb, 43.2 +/- 2.2 in the distal convoluted tubule, and 20.5 +/- 0.9 in the cortical collecting duct. For the group with moderate heart failure, UNaV was 0.35 +/- 0.02 (p less than 0.001 versus control), and aldosterone was 15.9 +/- 4.4 (p = NS versus control). Na,K-ATPase activity was unchanged in the proximal convoluted tubule, proximal straight tubule, medullary thick ascending limb, and cortical collecting duct, but it increased in the cortical thick ascending limb to 57.7 +/- 3.1 (p less than 0.001 versus control) and decreased in the distal convoluted tubule to 35.3 +/- 1.2 (p less than 0.005 versus control). For the group with severe heart failure, UNaV was 0.029 +/- 0.016 (p less than 0.001 versus control), and aldosterone was 186.0 +/- 14.8 (p less than 0.001 versus control).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Na,K-ATPase in isolated nephron segments in rats with experimental heart failure. 184 57

The association between arterial hypertension and obesity has been known for many years and demonstrated by epidemiological studies. The physiopathological mechanisms involved consist of increased extracellular volumes, hyperactivity of the sympathetic nervous system and the renin-angiotensin-aldosterone system, and abnormal ion exchanges between extra- and intracellular compartments. Recent studies have demonstrated an association between arterial hypertension and insulin resistance. Insulin resistance may well be the most important aetiological factor in this type of arterial hypertension as it stimulates both renal sodium reabsorption and sympathetic nervous system activity and reduces vascular Na-K-ATPase activity.
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PMID:[Arterial hypertension in patients with obesity. Role of hyperinsulinism and insulin resistance]. 209 34


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