RENOVASCULAR ADAPTIVE-CHANGES IN CHRONIC HYPOXIC POLYCYTHEMIA

Background Chronic hypoxia in rats produces polycythemia, and the plas ma fraction falls, reducing renal plasma flow (RPF) relative to renal blood how (RBF). Polycythemia also causes increased blood viscosity, w hich tends to reduce RBF and renal oxygen delivery. We studied how ren al regulation of electrolyte balance and renal tissue oxygenation (whi ch is crucial fur erythropoietin regulation) are maintained in rats du ring hypoxic exposure. Methods. Rats of two strains with differing pol ycythemic responses, with surgically implanted catheters Ln the urinar y bladder, femoral artery, and left renal and right external jugular v eins, were exposed to a simulated high altitude (0.5 atm) for 0, 1, 3, 14, and 30 days, after which RPF (para-aminohippurate clearance), glo merular filtration rate (GFR, polyfructosan clearance), hematocrit and blood gases were measured, and RBF, renal vascular resistance and hin drance (resistance/viscosity), renal oxygen delivery, and renal oxygen consumption were calculated. Results. During chronic hypoxia RBF incr eased, but RPF decreased because of the polycythemia. GFR remained nor mal because the filtration fraction (FF) increased. Renal vascular res istance decreased, and renal vascular hindrance decreased more markedl y. Renal oxygen delivery and consumption both increased. Conclusions. During chronic hypoxia GFR homeostasis apparently took precedence over RBF autoregulation. The large decrease in renal vascular hindrance su ggested that renal vascular remodeling contributes to GFR regulation. The reduced hindrance also prevented a vicious cycle of increasing pol ycythemia and blood viscosity, decreasing RBF, and increasing renal hy poxia and erythropoietin release.