EFFECTS OF IGF-I INFUSION ON GROWTH AND MUSCLE NA+-K+ PUMP CONCENTRATION IN K+-DEFICIENT RATS

K+-deficient rats and control rats were infused for 14 days with vehicle: acetic acid (AcA) or recombinant human insulin-like growth factor-I (IGF-I, 240 mug/day) by osmotic minipumps. IGF-I treatment of K+-deficient rats did not result in overall growth of carcass or muscles but in marked selective growth of adrenals (+42%) and spleen (+66%). In control rats, IGF-I induced increased body and muscle weight, tibia length, and thymus weight. K+ deficiency was associated with reduced serum IGF-I but unchanged thyroid status. IGF-I treatment of the K+-deficient rats restored serum IGF-I and decreased total 3,5,3'-triiodothyronine. In AcA-treated K+-deficient rats [H-3]ouabain binding site concentration decreased by 63 and 43% in soleus and extensor digitorum longus (EDL) muscle, respectively, compared with the AcA-treated controls. IGF-I had no effect on the [H-3]ouabain binding site concentration in the control group, but in K+-deficient rats a significant lowering of 26% was observed in EDL. K+ deficiency causes relative organ-specific resistance to the growth-promoting effects of IGF-I, comparable to the effects seen in protein-restricted rats. Reduced circulating IGF-I is not the only cause of the downregulation of Na+-K+ pumps in K+ deficiency, and IGF-I treatment of control animals in vivo has no stimulatory effect on the synthesis of Na+-K+ pumps.