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Biomedical subjects

I Singer

Publications and source records attributed to I Singer.

At least 73 records · Page 4Linked to original sources
PubMed1981

Subcellular localization of aldosterone-induced proteins in toad urinary bladders.

Paired toad urinary hemibladders were incubated with [35S]methionine in the presence (experimental) or absence (control) of aldosterone. Short-circuit current was used to monitor aldosterone-induced Na+ transport. Protein synthesis in epithelial cell subcellular fractions (cytosolic, microsomal, mitochondrial) was evaluated by gradient polyacrylamide gel electrophoresis and autoradiography. Aldosterone-induced proteins were identified in the cytosolic and microsomal fractions (70 000 and 15 000 daltons, respectively). These results represent the first demonstration of aldosterone-induced proteins in subcellular fractions of epithelial cells derived from single toad urinary hemibladders.

Aldosterone↗
PubMed1981

Internal potassium balance and the control of the plasma potassium concentration.

The plasma potassium concentration is determined both by external potassium balance and by the distribution of potassium between extracellular and intracellular fluid compartments, i.e., "internal potassium balance." Whenever external potassium balance is altered, the resultant change in the plasma potassium concentration is strongly influenced by concomitant alterations in internal potassium balance. Several factors alter internal potassium balance independently of changes in external balance. Acid-base disturbances produce shifts of potassium into or out of cells, but attempts to quantify these effects are not likely to be clinically useful. Hypertonicity produces a shift of potassium out of cells. Several hormones (insulin, aldosterone, catecholamines, glucagon, and growth hormone) may have roles in internal potassium balance. Digitalis and succinylcholine, by producing efflux of potassium from cells, may cause hyperkalemia. Potassium is released from skeletal muscle during exercise, causing an increase in the plasma potassium concentration. The periodic paralyses are associated with well-defined transient alterations in internal potassium balance.

Acid-Base Imbalance↗
PubMed1980

Drug therapy in renal failure: dosing guidelines for adults. Part II: sedatives, hypnotics, and tranquilizers; cardiovascular, antihypertensive, and diuretic agents; miscellaneous agents.

Data providing guidelines for drug use in adult patients with renal insufficiency are presented in tabular form with supporting references. The data are derived from the current medical literature. If specific information about a drug is unavailable or conflicting, emphasis is given to normal pharmacokinetic variables in arriving at recommendations for therapy. Nephrotoxicity or adverse effects in patients with renal disease are noted and adjustments for dialysis suggested.

Adult↗
PubMed1980

Drug therapy in renal failure: dosing guidelines for adults. Part I: Antimicrobial agents, analgesics.

Data are presented in tabular form that provide guidelines for drug use in adult patients with renal insufficiency. The data are derived from the current medical literature. If specific information about a drug is unavailable or conflicting, emphasis is given to normal pharmacokinetic variables in arriving at recommendations for therapy. Nephrotoxicity or adverse effects in patients with renal disease are noted and adjustments for dialysis suggested.

Analgesics↗
PubMed1979

Effects of tetracyclines on aldosterone- and insulin-mediated Na+ transport in the toad urinary bladder.

The effect of oxytetracycline and demethylchlortetracycline on aldosterone- and insulin-mediated Na+ transport (short-circuit current) were examined in toad urinary bladders mounted in modified Ussing chambers. Oxytetracycline had little or no effect on either basal or aldosterone-mediated Na+ transport. In contrast, demethylchlortetracycline markedly inhibited both basal and aldosterone-mediated Na+ transport. Furthermore, demethylchlortetracycline inhibited the aldosterone response significantly out of proportion to its effects on basal Na+ transport. Neither of the drugs had an effect on insulin-mediated Na+ transport. Consequently, the natriuresis observed in certain patients treated with demethylchlortetracyline may be related to drug-induced renal resistance to the effects of aldosterone.

Aldosterone↗
PubMed1979

Disposition of intravenous potassium in anuric man: a kinetic analysis.

The disposition of a constant-rate (0.3 mEq/kg/hr) intravenous potassium load was studied in anuric, chronic hemodialysis patients. Changes in plasma potassium concentration could be adequately described by a two-compartment kinetic model under both isohydric conditions and during acute metabolic alkalosis. From 63 to 92% of the infused potassium left the extracellular fluid (ECF) in isohydric studies, and from 73 to 97% left the ECF in alkalanizing studies. Cellular uptake of the infused potassium was less when the plasma potassium concentration was higher. Plasma aldosterone levels rose but insulin levels did not increase during infusions. In a juvenile-onset diabetic subject, the impairment of cellular potassium uptake at higher plasma potassium was magnified so that infused potassium was virtually confined to the ECF compartment until exogenous insulin was given. This implies a permissive rather than a regulatory role for endogenous insulin in facilitating cellular entry of excess potassium.

Anuria↗
PubMed1978

Superiority of demeclocycline over lithium in the treatment of chronic syndrome of inappropriate secretion of antidiuretic hormone.

We evaluated demeclocycline and lithium therapy in 10 patients with the syndrome of inappropriate secretion of antidiuretic hormone. Despite severe water restriction, all patients had hyponatremia (mean +/- S.E.M. serum sodium of 122 +/- 1.1 meq per liter) and elevated urine osmolality (744 +/- 59 mOsm per kilogram) before treatment. Demeclocycline (600 to 1200 mg daily) restored serum sodium concentration to 139 +/- 1.1 meq per liter within five to 14 days, permitting unrestricted water intake in all patients. In three patients given lithium carbonate (900 mg daily) the serum sodium concentration, urine osmolality and urine volume were unchanged; since two patients had adverse central-nervous-system symptoms during lithium therapy, further study of this agent was abandoned. A patient with an unusual 22-year history of the syndrome was unresponsive to lithium, whereas long-term treatment with demeclocyline was markedly effective. Demeclocycline is superior to lithium in the treatment of the syndrome and may obviate the need for severe water restriction.

Adult↗
PubMed1978

Tetracycline-induced inhibition of Na+ transport in the toad urinary bladder.

The effects of three tetracyclines, demethylchlortetracycline (DMC), minocycline (MNC), and oxytetracycline (OTC), on Na+ transport (measured as short-circuit current) were examined in toad urinary bladders mounted in modified Ussing chambers. During a 1-h incubation period serosal DMC (but not MNC or OTC) inhibited basal Na+ transport, whereas MNC (but not DMC or OTC) inhibited ADH-stimulated Na+ transport. MNC also inhibited cyclic AMP-stimulated Na+ transport. During longer incubation periods all three drugs inhibited basal Na+ transport. The DMC-induced inhibition of basal Na+ transport and the MNC-induced inhibition of ADH-stimulated Na+ transport were paralleled by an inhibition of the active conductance of the bladders. Thus, although all three drugs inhibit basal Na+ transport, only MNC inhibits ADH-stimulated Na+ transport. This effect does not correlate with the known effects of the tetracyclines on ADH-stimulated water flow or with drug-protein binding, and may be related to the greater lipid solubility of MNC.

Animals↗
PubMed1977

Insulin-mediated Na+ transport in the toad urinary bladder.

The characteristics of insulin-induced Na+ transport in the toad urinary bladder were determined and compared to those of aldosterone. Bladders were mounted in modified Ussing chambers, and standard short-circuit current techniques were employed to measure transepithelial Na+ transport. Insulin added to the serosal medium is much more effective than insulin added to the mucosal medium. Serosal insulin concentrations from 10(1) to 10(3) muU/ml increase both the initial rate and the final level of Na+ transport achieved, whereas concentrations from 10(3) to 10(5) muU/ml increase only the initial rate of Na+ transport. Insulin-induced Na+ transport probably does not require glucose. Both insulin- and aldosterone-induced Na+ transport are directly proportional to serosal (but not mucosal) K+ concentration over the physiologic range (2.0-7.0 meq/liter). However, cycloheximide abolishes aldosterone- but not insulin-induced Na+ transport. In addition, insulin stimulates Na+ transport after a maximal response to aldosterone, and aldosterone stimulates Na+ transport after a maximal response to insulin. Thus, although they have several similar characteristics, insulin and aldosterone have at least partially independent mechanisms of action on Na+ transport in the toad urinary bladder.

Aldosterone↗
PubMed1977

Guidelines for drug therapy in renal failure.

Five tables are presented that provide guidelines for drug usage in patients with renal insufficiency. The data are derived from the current medical literature. If specific information about a drug is unavailable, emphasis is given to normal pharmacokinetic variables in arriving at recommendations for therapy. Nephrotoxicity of adverse effects in patients with renal disease are noted and adjustments for dialysis suggested.

Acute Kidney Injury↗
PubMed1976

Hysterical polydipsia (compulsive water drinking) in children.

Two patients had entirely different clinical presentations of hysterical polydipsia: convulsions and coma in a 5-year-old boy with intrinsic renal disease and a single kidney, and abnormal behavior in a 3-year-old girl with normal kidneys. In neither case was the correct diagnosis made on initial evaluation. Physiological studies demonstrated primary polydipsia to be responsible for both clinical presentations. The differential diagnosis of polydipsia and polyuria is reviewed, and the nonuniform presentation of hysterical polydipsia is emphasized. In children with intrinsic renal disease, hysterical polydipsia may be life-threatening.

Child, Preschool↗
PubMed1976

Renal failure, hemodialysis, and nafcillin kinetics.

Nafcillin (N) pharmacokinetics was studied in 27 subjectswith and without renal failure (RF) (determined by endogenous creatinine clearance, Ccr). Elimination rate constants (K) were calculated from serial serum levels of N measured from 2 to 12 hr after a single 500-mg intramuscular injection. Only 4 of 9 hemodialysis patients had measurable levels of N at 24 hr. The K values for the groups with normal renal function,moderate RF, severe RF, and on hemodialysis were 0.477 hr(-1), 0.432 hr (1), 0.369 hr(-1), and 0.306 hr (-1), respectively...

Adult↗