ABSTRACT
When proximal tubules are immersed in hypotonic medium, they quickly swell to a peak volume. In a second, slower phase, termed volume regulatory decrease (VRD), they shrink as K, anion, and water leave the cells. We investigated the role of the cytoskeleton during this biphasic hypotonic volume regulatory response. Isolated, collapsed rabbit proximal convoluted tubules (PCT) were crimped tightly between two pipettes, and their volume was assessed optically. PCT volume increased to a peak 70-80% above baseline on sudden immersion in dilute medium (150 mosmol/kgH2O). After completing VRD, control tubules had regulated their volume 73 +/- 2% back toward baseline. Tubules exposed to the microtubule inhibitor vincristine (5 microM) regulated 75 +/- 2%. Tubules exposed to the microfilament inhibitor cytochalasin B (50 microM) regulated less (57 +/- 5%), and tubules exposed to both inhibitors regulated only 39 +/- 3% (P less than 0.01 vs. control). Hypotonic VRD was unimpaired in PCT loaded with NaCl by prior exposure to ouabain but was significantly reduced by cytochalasin B. We conclude that VRD is not cation specific and that intact microtubules and microfilaments play a synergistic role in the VRD of rabbit PCT in hyposmotic medium.
Subject(s)
Cytoskeleton/physiology , Kidney Tubules, Proximal/metabolism , Animals , Culture Media , Cytoskeletal Proteins/metabolism , Female , Kidney Tubules, Proximal/drug effects , Kidney Tubules, Proximal/ultrastructure , Microscopy, Fluorescence , Osmolar Concentration , Ouabain/pharmacology , RabbitsABSTRACT
Minor physical anomalies (MPAs) are congenital abnormalities of body structure which reflect fetal maldevelopment. They originate in the same embryonic layer that produces the central nervous system, and it is reasoned that MPAs are markers of nervous system anomalies. High MPA counts have been associated with hyperactive behavior in normal and clinical populations of boys, and with inhibited behavior in normal groups of girls. The present sample of children from a longitudinal study of a Danish birth cohort show no significant sex differences in mean number of MPAs, but the male hyperactivity-MPA relation and the female inhibition-MPA relation is supported in this non-clinical sample. MPAs are not recommended for use in clinical screening or diagnosis at this time, but the evidence of a congenital, biological component to hyperactive behavior may eventually have useful implications for prevention and/or intervention.
