The dopamine (DA) uptake over a concentration range from 0.03 to 100 microM was studied in S1 fractions of the rat striatum prepared from control rats and those exposed for 14 h to hypobaric hypoxia. The uptake exhibited non-Michaelis-Menten kinetics, which were evaluated by applying an equation assuming two transport sites. The high-affinity uptake site was characterized by an apparent Michaelis-Menten constant of 0.47 microM and an apparent maximal transport rate of 113 pmol/mg protein/30 s. The respective constants of the low-affinity uptake site were 52.8 microM and 1490 pmol/mg protein/30 s. One hour after hypoxia kinetic constants of the high-affinity uptake were unchanged but the maximal transport rate of the low-affinity uptake was increased by 50%. The elevated low-affinity uptake capacity may represent a means of adaptation to hypoxia allowing a faster removal of high extracellular concentrations of DA.

Animals↗

PubMedDate not supplied

Metabolic rates of 4-hydroxynonenal in tubular and mesangial cells of the kidney.

The degradation of the lipid peroxidation product 4-hydroxynonenal (HNE) in primary cultures of kidney tubular and mesangial cells was determined. Using various initial concentrations of the aldehyde a decline of cellular viability was found. Mesangial cells were more susceptible to the toxic effects of HNE. In consumption studies of HNE the decline of the exogenously added aldehyde was comparable in both cell types after addition of 10 and 1 micromol HNE/l. After addition of 100 micromol/l aldehyde a drastically lower HNE degrading capacity was found in mesangial cells as compared to tubular cells. The loss in the HNE degrading capacity was accompanied by an increased formation of HNE-protein aggregates as demonstrated by immunoblots. Therefore, we concluded that the low ability of mesangial cells to degrade HNE may be a factor of the toxicity of free radicals on the kidney.

Aldehydes↗

PubMedDate not supplied

Identification of an external NADH oxidase in rat kidney cortex mitochondria.

Intact rat kidney cortex mitochondria oxidize external NADH and NADPH. Basal NADH oxidation of mitochondria, but not basal NADPH oxidation, is stimulated by hexammine-ruthenium (HR). 10.7 mumol/l HR induce 50% of the maximal NADH-oxidizing activity and amounted to 169 nmol NADH/min/mg of mitochondrial protein. The HR-stimulated NADH oxidation involves a stoichiometric 1:1 oxygen consumption. The electron transfer from NADH to oxygen does not occur via the respiratory chain complex I, but is connected with a superoxide anion radical formation. Experiments with intact mitochondria, submitochondrial particles and inner mitochondrial membranes show that rat kidney cortex mitochondria possess a NADH oxidase localized on the outer surface of the inner mitochondrial membrane.

Animals↗

PubMedDate not supplied

Individual assessment of antihypertensive response by self-starting cumulative sums.

A self-interpreted control chart, on an individualized basis, assesses the effect of a switch from beta-blockers to an angiotensin-converting enzyme (ACE)-inhibitor in a patient with occasional blood pressure (BP) excess. In dense and long data series, the BP and heart rate (HR) of this patient respond to the change in treatment by the test criterion of a self-starting Cumulative Sum (cusum), which reaches values outside a decision interval with a lowering of BP and an increase in HR and vice versa, at least for BP, after treatment cessation. Thereafter, minimal sampling requirements are sought in the same data by applying the same control chart approach to decimated data. Skeleton sampling schemes in a system of chronobiologic self-analysis and interpretation of manually recorded data obtained at strategically placed times (established on the basis of data decimations) could complement control charts that are used on a home computer or preferably would be built into the output of ambulatory monitors used at the outset as a minimum and routinely as an optimum.

Adrenergic beta-Antagonists↗