Effects of acute anoxia on renal transport processes.
Acute disruption of the renal blood supply has been shown by several workers to alter renal cortical metabolic functions and some transport processes. The present study was designed to examine acute ischemic effects on transport functions for both organic and inorganic substances. Acute clamping of the renal artery, renal vein, and ureter for 45 min produces a reversible disruption of tissue electrolyte and water balance. Longer occlusion appeared to produce irreversible effects. Alpha-Aminoisobutyrate (AIB) and lactate-stimulated rho-aminohippurate (PAH) transport were altered selectively by the 45-min occlusion. A longer occlusion period also depressed base-line PAH and tetraethylammonium (TEA) transport. Some of the depression of the organic compound transport functions are reversible. Renal cortical oxygen consumption measured in vitro was affected minimally.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000621:Aminoisobutyric Acids / Q000378:metabolism; D000818:Animals; D001692:Biological Transport; D004573:Electrolytes / Q000378:metabolism; D005260:Female; D000860:Hypoxia / Q000378:metabolism*; D007672:Kidney Cortex / Q000378:metabolism*; D007773:Lactates / Q000378:metabolism; D008297:Male; D010101:Oxygen Consumption; D051381:Rats; D013757:Tetraethylammonium Compounds / Q000378:metabolism; D013997:Time Factors; D010130:p-Aminohippuric Acid / Q000378:metabolism
D000621:Aminoisobutyric Acids; D004573:Electrolytes; D007773:Lactates; D013757:Tetraethylammonium Compounds; D000255:Adenosine Triphosphate; D010130:p-Aminohippuric Acid