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F H Epstein

Publications and source records attributed to F H Epstein.

At least 235 records · Page 13Linked to original sources
PubMed1976

Multiple pumps for sodium reabsorption by the perfused kidney.

Several distinct transport mechanisms responsible for sodium reabsorption by the rat kidney can be identified by studying the function of isolated perfused kidneys. Approximately one-half of the fractional sodium reabsorption by the isolated perfused rat kidney appears to depend on Na-K-adenosine triphosphatase (AT-Pase) and is inhibited by ouabain. About 10 to 20% is associated with the reabsorption of bicarbonate and is blocked by acetazolamide. This fraction of transported sodium is unaffected by ouabain and therefore does not involve Na-K-ATPase. Neither furosemide nor ethacrynic acid produce further inhibition of sodium reabsorption in a kidney already exposed to ouabain and acetazolamide. Most of the residual transport of sodium is inhibited by cooling the perfused kidney, suggesting that it is powered by metabolic rather than physical sources of energy.

Acetazolamide↗
PubMed1976

Genetics of ischaemic heart disease.

Coronary heart disease, especially when it affects younger individuals, tends to cluster in families. Known risk factors occur in 50-75% of patients with myocardial infarction. Yet commonly occurring risk factors are not strongly inherited, and the familial aggregation of coronary heart diseas may not be attributable to familial resemblance in serum cholesterol and blood pressure levels. Alternatively, such aggregation may be due to unknown familial risk factors. Nevertheless, screening of relatives of individuals with evident risk factors is of importance, and environmental manipulation is likely to be of value in prevention of coronary heart disease.

Cholesterol↗
PubMed1976

Relation between Na-K-ATPase activity and respiratory rate in the rat kidney.

The relation between Na-k-ATPase activity in homogenates of rat kidney and oxygen consumption in kidney slices was studied by employing different physiological maneuvers known to change the activity of renal Na-K-ATPase. Treatment of euthyroid rats with 3,5,3'-triiodo-1-thyronine increased Na-K-ATPase activity, sodium-dependent oxygen consumption (QO2[t]), and para-aminohippurate (PAH) accumulation by kidney slices without changing glomerular filtration rate or net sodium reabsorption by the intact kidney. Treatment with methylprednisolone also increased Na-K-ATPase, QO2[t], and PAH transport. Chronic potassium loading, on the other hand, increased renal Na-K-ATPase to the same degree as the first two procedures, but QO2[t] and PAH accumulation were unchanged. Partial nephrectomy induced an increase in the activity of Na-K-ATPase in homogenates of the remaining kidney fragment, but QO2[t] did not change significantly and PAH uptake was unaltered. An increase in the activity of Na-K-ATPase in kidney homogenates is therefore not necessarily associated with a parallel change in oxygen consumption by the intact cell.

Adenosine Triphosphatases↗
PubMed1975

Metabolic adjustments of the kidney involved in the adaptation to potassium loading.

Potassium adaptation involves the development of the ability of the kidneys to secrete large amounts of potassium into the urine. This is accompanied by an adaptive increase in the specific activity of sodium-potassium-ATPase in the kidney, predominantly in the medulla and the papilla, but also involving the cortex. It is likely that these changes are localized to the distal tubule and are especially marked in the collecting ducts although there is no direct evidence bearing on this. Net secretion of potassium in isolated kidneys taken from chronically potassium loaded animals is completely eliminated when ouabain, a specific inhibitor of sodium-potassium-ATPase, is added to the perfusion medium. The secretion of potassium appears also to depend critically on the availability of glucose as substrate.

Acute Kidney Injury↗
PubMed1975

Bicarbonate and sodium reabsorption by the isolated perfused kidney.

The role of bicarbonate reabsorption and of transtubular chloride gradients in the bulk reabsorption of sodium and water by renal tubules can be tested in the isolated perfused kidney by perfusing with a medium from which bicarbonate has been omitted. Perfusion of the isolated rat kidney with an artificial medium in which bicarbonate is replaced by chloride results in a fall in fractional reabsorption of sodium from 97 to 84%. Stepwise restoration of bicarbonate concentration in the perfusion medium to 25 meq/liter is associated with a parallel recovery of sodium reabsorption to control levels. Inhibition of bicarbonate reabsorption with acetazolamide produces a slightly smaller reduction in sodium reabsorption (97-89%), an effect not seen in the absence of bicarbonate. Acetazolamide greatly increases phosphate excretion and free water clearance in a way consistent with suppression of proximal tubular reabsorption. By contrast, simple omission of bicarbonate from the perfusing medium does not alter phosphaturia or free water clearance. Reabsorption of bicarbonate appears to account for a fraction of sodium reabsorption roughly equivalent to the proportion of sodium associated stoichiometrically with bicarbonate in the glomerule filtrate. The data do not support the hypothesis that the development of a transtubular chloride gradient is critically important for the reabsorption of a large fraction of the glomerular filtrate.

Acetazolamide↗
PubMed1975

Thiocyanate inhibition of ATPase and its relationship to anion transport.

Adenosine triphosphatase activity not dependent on sodium or potassium but inhibited by thiocyanate is present in broken-cell homogenates of eel gill and rat kidney. This enzymatic property is predominantly associated with mitochondria, although thiocyanate-inhibited ATPase can also be detected in microsomes with little or no mitochondrial contamination as measured by the activity of the mitochondrial marker enzyme succinic dehydrogenase. When eels are transferred from fresh to salf water, thus increasing active outward transport of chloride across the gill, the thiocyanate-inhibited ATPase of gill microsomes does not change, though the activities of succinic dehydrogenase and Na-K-ATPase in gill homogenates are augmented. The thiocyanate-inhibited ATPase of homogenates of outer renal medulla does not differ from that of renal cortex, in contrast to Na-k-atpase which is higher in renal medulla than in cortex. The data do not support a role for thiocyanate-inhibited ATPase in active chloride transport by epithelial tissues.

Adenosine Triphosphatases↗
PubMed1975

Potassium adaptation and Na-K-ATPase activity in mucosa of colon.

The specific activity of sodium-potassium-activated adenosine triphosphatase in the mucosa of the colon rises when the dietary load of potassium is increased. The change in enzymatic activity depends on the presence of intact adrenal glands, since adrenalectomy abolishes the response of Na-K-ATPase to potassium loading. The increased secretory rate of aldosterone normally evoked by potassium loading appears to mediate at least in part of the effect of potassium loading, since aldosterone induces a discernible increase in the specific activity of Na-K-ATPase in the colon of adrenalectomized rats.

Adenosine Triphosphatases↗
PubMed1975

An in vitro inhibitor of Na-K-ATPase present in an adenosinetriphosphate preparation.

An in vitro inhibitor of Na-K-ATPase was discovered in a commonly used preparation of ATP made by the Sigma Chemical Company, St. Louis, Mo. (Sigma grade ATP). As measured by a reliable and widely used assay system in which phosphate liberation in measured colorimetrically, Na-K-ATPase activity in the rat kidney, small intestine and colon was about 50% lower then Sigma grade ATP was used as substrate as compared to another Sigma Chemical Company product II ATP. Mg-ATPase and adenylate cyclase assays were unaffected by substituting Sigma grade for grade II ATP. The inhibitor of Na-K-ATPase could not be identified. Sigma grade ATP probably should not be used when measuring the activity of Na-K-ATPase in the rat kidney, small intestine, or colon.

Adenosine Triphosphatases↗
PubMed1975

Potassium transport by the isolated perfused kidney.

Rat kidneys perfused outside of the body with an artificial medium are able to increase their fractional excretion of potassium in response to a rising concentration of potassium in the medium but never show net secretion of potassium. By contrast, isolated perfused kidneys from chronically potassium-loaded rats regularly secrete potassium in excess of the amount filtered. Ouabain completely blocks the secretion of potassium by these isolated kidneys, suggesting that Na-K-ATPase mediates potassium secretion by potassium-adapted rats. Neither sodium deprivation, pretreatment with deoxycorticosterone, nor pretreatment with methylprednisolone prepared the kidney to secrete potassium, despite stimulation of Na-K-ATPase activity in cortex or outer medulla. Potassium loading was the only maneuver tested that increased the activity of Na-Katpase in the inner medulla (white papilla) and also produced potassium secretion by the isolated kidney. Surgical ablation of the papilla abolished the net secretion of potassium normally seen in perfused kidneys of potassium-adapted rats, thus underlining the importance of the papilla in the process of potassium adaptation.

Adaptation, Physiological↗