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The microtubule-stabilizing ability of a major HeLa cell microtubule-associated protein (MAP4) was previously observed to be decreased by cdc2 kinase. It was found that cdc2 kinase is the major M-phase MAP4 kinase and two phosphorylation sites within the proline-rich domain of MAP4 were determined. Metabolic 32P labeling revealed increased phosphorylation of MAP4 at mitosis. A specific inhibitor of cdc2 kinase, butyrolactone I, impeded phosphorylation of MAP4 both in mitotic HeLa cells and in the mitotic HeLa cell extract.

Protein-deprived male Wistar rats were analyzed after infusion of hypertonic sodium and urea to determine the effects of protein deprivation on renal medullary organic osmolyte content and urea concentration. Protein-deprived Wistar rats exhibited low levels of sodium-dependent myo-inositol transporter (SMIT) messenger ribonucleic acid expression (mRNA). Infusion of NaCl and urea in the renal medulla did not alter the levels of SMIT mRNA in protein-deprived rats due to reduced levels of myo-inositol.

Analysis of the influence of oral administration of vasopressin V1 and /or V2 antagonists on organic osmolytes in rat renal inner medulla shows that these antagonists change the accumulation of a few osmolytes. Different organic osmolytes exhibit different responses to the V1 or V2 receptor antagonists. V2 receptor suppresses taurine accumulation while V1 receptor increases the accumulation of betaine.

Experimental analysis of the influence of potassium depletion on osmolytes in the renal medulla of rats shows that potassium depletion leads to defects in the renal concentration, which are different for polyuria and polydipsia, and decreased accumulation of osmolytes. High sodium extracellular osmolality inhibits the accumulation of betaine, sorbitol and taurine in inner medulla.