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Biomedical subjects

C N Corder

Publications and source records attributed to C N Corder.

At least 55 records · Page 3Linked to original sources
PubMed1977

Purification of the (Na+ + K+)-adenosine triphosphatase from human renal tissue.

(Na+ + K+)-ATPase (ATP phosphohydrolase, EC 3.6.1.3) was purified from human cadaver renal tissue and exhibited a linear reaction rate with time. 100 g of whole kidney would yield 1--3.5 mg protein with a specific activity of 50--200 mol - kg-1 - h-1 for (Na+ + K+)-ATPase. The preparation was completely inhibited by 100 micronM ouabain with a Ki of 1.8 micronM. K+-dependent phosphatase increased during purification of (Na+ + K+)-ATPase to 7.8 mol - kg-1 - h-1. There was no detectable Mg2+-ATPase in the final preparation. Sodium dodecyl sulfate-polyacrylamide disc gel electrophoresis yielded three protein peaks of 117 000, 92 500, and 56 000 daltons. The peptide band corresponding to 92 500 daltons underwent an Na+-dependent phosphorylation with [gamma-32P]-ATP. The band at 56 000 daltons stained for glycoprotein. The Km for ATP was 0.38 mM and that for Mg2+ was 0.5 mM. The formation of ADP and inorganic phosphate from ATP was stoichiometric. The Km for Na+ in the presence of 20 mM K+ was 16 mM and the Km for K+ in the presence of 100 mM Na+ was 1.5 mM. The temperature optimum was 51degrees C and the pH optimum was 7.0. (Na+ + K+)-ATPase in whole homogenate, microsomes, and NaI-treated microsomes exhibited a slowing of reaction rate (non-linearity) with time such that the enzyme was inactive by 10--15 min of reaction. This non-linearity was eliminated during purification. The significance is discussed.

Adenosine Triphosphatases↗
PubMed1977

Aldose reductase and sorbitol dehydrogenase distribution in rat kidney.

The sorbitol pathway catalyzes the conversion of glucose to fructose via the intermediate sorbitol. It consists of aldose reductase (AR) and sorbitol dehydrogenase (SDH). In adult (44 day) kidney zones, AR was highest in the outer medulla. In substructures AR was highest in distal convoluted tubule. The AR was greatest in newborn and 8-day zones of developing rat kidney. Acute alloxan diabetes was associated with decreased AR in small arteries, but not glomeruli. The SDH was lowest in outer medulla. It was most active in glomeruli and distal convoluted tubules. The diabetic state leads to no change of SDH in arteries but an increase in glomeruli. SDH increased with development. This study demonstrates AR and SDH in substructures of the kidney. The pathway is present in developing kidney. In diabetes the enzymatic changes would tend to decrease accumulation of sorbitol.

Alcohol Oxidoreductases↗
PubMed1977

Postural hypotension: adrenergic responsivity and levodopa therapy.

Four subjects with orthostatic hypotension were given intravenous infusions of methoxamine and isoproterenol. Methoxamine caused an elevation in systolic blood pressure. Isoproterenol resulted in a fall in blood pressure in three of the subjects. The heart rate decreased with methoxamine, but increased with isoproterenol. The responsivity in orthostatic hypotension was compatible with denervation supersensitivity. These effects were compared with the responsivity to methoxamine and isoproterenol of five labile hypertensives. Two patients with severe orthostatic hypotension were treated with regimens including levodopa. Levodopa alone would further aggravate postural hypotension. But in one subject given levodopa, ephedrine, and fludrocortisone and in the other managed on levodopa, tranylcypromine, and fludrocortisone, symptomatic orthostatic hypotension was successfully eliminated. These results support the usefulness of levodopa, in combination with adrenergic agents, as a therapeutic measure for advanced forms of orthostatic hypotension.

Adrenergic Fibers↗
PubMed1977

Aldose reductase and sorbitol dehydrogenase distribution in substructures of normal and diabetic rat lens.

Aldose reductase (AR) and sorbitol dehydrogenase (SDH) make up the sorbitol pathway, which has been implicated in the pathogenesis of sugar cataracts. The levels of the two enzymes were determined with quantitative histochemical techniques in the epithelium, cortex, and nucleus of normal and diabetic rat lenses. The ratio of activity of AR to SDH was found to be nearly 50 to 1 in all substructures. This would strongly favor sorbitol accumulation and subsequent cataract formation.

Alcohol Oxidoreductases↗
PubMed1977

High-performance liquid chromatographic radioenzymatic assay for plasma catecholamines.

A new assay method for plasma CA's requiring only 50 microliter has been developed, which uses HPLC. The NE, D, and E compounds found in plasma are radioactively o-methylated with 3H-SAM by the reaction of COMT. The reaction is terminated and a standard mixture of nonradioactive o-methylated analogues of NE, D, and E is addded to act as a carrier. Following separation by HPLC, the NMN, 3-MOT, and MN radioactive peaks are collected which represent NE, D, and E, respectively. Then MNM and MN are oxidized to vanillin, and 3-MOT is acetylated. The products are subsequently separated by solvent extraction. This is necessary in order to avoid high radioactive blanks and to allow quantitation of the radioactivity by liquid scintillation spectrometry. The mean supine levels of NE, D, and E in normal subjects were respectively 182, 33, and 87 pg/ml of plasma. Similar assays on patients with pheochromocytoma revealed 797, 80, and 470 pg/ml.

Adult↗
PubMed1975

Fluorometric assay of bethanidine in plasma.

A fluorometric method for determining bethanidine in blood plasma is described. The bethanidine is extracted into chloroform, a drug-dye complex with eosin Y is formed, and the fluorescence is measured (excitation, 535 nm; fluorescence, 560 nm). The assay detects 0.02 muM bethanidine (4 ng/ml) in plasma. The relative fluorescence of several body constituents and antihypertensive drugs is negligible. The plasma levels of bethanidine in four hypertensive patients receiving this drug were measured.

Animals↗
PubMed1975

Histochemical measurements of rat kidney hexokinase.

HK has been measured in substructures of the developing rat nephron. Reactions were carried on samples dissected from freeze dried kidney and assayed in 1 mul reaction volume utilizing the "oil-well" technique. Samples from 4 days prenatal to 44-day adult were analyzed. Activity during development decreased in G, PCT, and it increased in ALH. There was little change in PRT, DCT and CT. Activity in small arteries decreased.

Adenosine Triphosphate↗
PubMedDate not supplied

Bethanidine dose, plasma levels, and antihypertensive effects.

Bethanidine dose, plasma levels, and hypotensive effects were evaluated in twelve hypertensive patients. Diuretic therapy with benzthiazide was started two weeks before and continued during the study. Bethanidine was given three times daily. After two to 12 months of therapy in 11 of the patients, the mean standing diastolic pressure was reduced from 112 to 91 mm Hg. The mean total daily bethanidine dose was 79 mg (range 30--150 mg). The mean plasma bethanidine was 0.65 micrometer (range 0.1--2.8 micrometer), which correlated with the bethanidine dose. There was less correlation between dose and antihypertensive effect. The effects of sudden withdrawal from chronic bethanidine dosing were observed in six patients. The orthostatic effect of bethanidine was lost within 12 hours, but the half-time of elimination of bethanidine from plasma was 39 hours. Based upon the present findings, recommendations are presented for initiation and maintenance of antihypertensive therapy with bethanidine.

Adult↗
PubMedDate not supplied

Bethanidine elimination from plasma.

Bethanidine was administered intravenously to six hypertensive patients with normal renal function and five hypertensive patients with renal impairment. After administration of 0.7 mumole/kg, blood was sampled at frequent intervals for measurement of plasma bethanidine. The plasma levels were analyzed on a three-compartment exponential open-model system. The second rapid elimination phase (beta) had a half-time of 3.4 hours in normal subjects and was insignificantly prolonged to 16.4 hours in renal impairment. There was an extended terminal elimination phase of 90 and 70 hours for normals and impaired, respectfully. The volume of distribution at pseudoequilibrium was 2.8 and 1.6 liters/kg, respectively, suggesting significant sequestration of the drug in body tissues. The pharmacokinetic constants of bethanidine in normal and impaired renal functions were similar.

Adult↗
PubMedDate not supplied

Hemodynamic effects of calcitonin in the normal rat.

Calcitonin (CT) was administered acutely (IV 4-8 U/kg) and chronically (SC 2 U/kg/day x 150 day) to normal male rats. Measurements included heart rate (HR), mean blood pressure (MBP), cardiac index (CI), peripheral vascular resistance (PVR), and stroke volume index (SVI). The MBP was higher in CT rats examined under pentobarbital anesthesia. Upon awakening from anesthesia, rats chronically on CT exhibited impaired recovery of CI and SVI. Hemodynamic effects were not seen in rats acutely treated with CT. Heart weight was unchanged in chronic treatment with CT. Therefore, CT had minimal hemodynamic effects in the normal male rat.

Anesthesia, General↗