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Biomedical subjects

K Thurau

Publications and source records attributed to K Thurau.

149 records · Page 9Linked to original sources
PubMedDate not supplied

Cellular osmoregulation in renal medulla.

Cells of the renal medulla adapt osmotically to varying external electrolyte concentrations mainly by changing the intracellular content of small organic osmoeffectors (osmolytes) such as sorbitol, inositol and trimethylamines. This implies that despite extreme variations in extracellular tonicity the intracellular concentrations of monovalent electrolytes are stabilized at levels optimal for enzyme function and cell metabolism. In contrast to inorganic electrolytes these organic osmolytes are metabolically neutral and thus do not affect cell metabolism. In addition, some of these organic osmoeffectors, the trimethylamine compounds, are known to counteract the deleterious effects of high urea concentrations (prevailing in antidiuresis) on structure and function of cell proteins.

Animals↗
PubMedDate not supplied

Atrial natriuretic factor infusion following acute renal ischemia in anesthetized dogs.

Atrial natriuretic factor (ANF) has been shown to be effective in reversing renal functional impairments following renal ischemia. We studied the effects of a nonhypotensive intravenous ANF infusion (100 ng/min x kgBW, 60 min) after 90 min unilateral renal arterial occlusion in anesthetized dogs with an intact contralateral kidney. ANF plasma levels remained unchanged in controls (group 1) and increased in ANF-infused animals (group 2) from 22 +/- 3 to 552 +/- 124 pg/ml. Blood pressure increased in both groups during renal ischemia, but returned to control values in group 2 when ANF infusion was started. Plasma vasopressin did not change in group 1, but increased in group 2 (0.77 +/- 0.29 vs. 1.10 +/- 0.49 pg/ml) after terminating ANF infusion. The postischemic fall in creatinine clearance (CCr), filtration fraction (FF) and renal blood flow (RBF) was prevented by infusion of ANF (CCr: group 1, 0.16 +/- 0.05 vs. group 2, 1.01 +/- 0.25 ml/min x kgBW; FF: group 1, 4.0 +/- 1.6 vs group 2, 14.1 +/- 4.1%; RBF: group 1, 6.0 +/- 1.2 vs. group 2, 9.2 +/- 1.6 ml/min x kgBW); however, the effects were limited to the time of infusion and the postischemic increase in urinary excretion of the proximal tubular enzyme N-acetyl-beta-D-glucosaminidase (NAG; group 1, 317.7 +/- 163.6 vs. group 2, 672.4 +/- 245.7 microU/min x kgBW) was not improved by ANF. Our data suggest that infusion of ANF transiently reverses postischemic renal impairment. However, the failure to demonstrate a sustained postischemic improvement of renal functional parameters and to ameliorate massive NAG excretion casts doubt on the benefit of ANF infusion in preventing cellular damage.

Acetylglucosaminidase↗