No abstract

The distribution of filaments was studied in hypertrophied rabbit vascular smooth muscle . Hypertrophy was induced by partial ligation of the portal-anterior mesenteric vein . 14 d after ligation, there was an approximately threefold increase in the number of intermediate filaments per cross-sectional area, as compared to control values . The actin :intermediate:myosin filament ratio was 15 :1 .1 :1 in control and 15 :3 .5 :0 .5 in hypertrophied portal-anterior mesentric vein vascular smooth muscle . Comparison of the filament ratios with the increase in volume density of the hypertrophied cells suggests that the number of myosin filaments per cell profile remained approximately the same as in controls, whereas the number of actin filaments increased in proportion to the increase in cell volume .Intermediate (10 nm diameter) filaments are ubiquitous components ofmost, if not all, eukaryotic cells (see reference 39 for review) . In nonneural tissue, they were first described by Ishikawa et al. (35) in cultured cells and distinguished from actin filaments through the difference in size and the failure of the 10-nm filaments to bind the heavy meromyosin subfragment of myosin. Recent studies have shown that the major component ofthe intermediate filaments in muscle is a protein of 50,000-55,000 mol wt (15). In nonmuscle cells, other than nerve, a related protein of slightly higher mass (55,000-58,000 daltons) forms the 10-nm filaments, although the two proteins may also coexist in the same cell (5,20,24). A marked increase in the number of intermediate filaments, frequently in the form ofcables, can be induced in muscle and in other cells by drugs such as cytochalasin B and Colcemid (CIBA Pharmaceutical Co., Summit, N. J.) (4,29,33,34,38,55,56) .In normal adult mammalian smooth muscle, intermediate filaments generally surround dense bodies on which actin filaments insert (2) . Intermediate filaments are very numerous in cultured vascular (45-47) and other smooth muscles (11)(12)(13)60). In previous studies of normal adult vascular smooth muscle, occasional cells were found containing massive quantities ofintermediate filaments that appeared to displace the normal actin and myosin filament lattice (50, 52) . Although it was recognized that such proliferation of intermediate filaments in adult smooth muscle represented some form of cellular pathology, its specific cause was not known . We now show that a large increase in the number of intermediate filaments in vascular smooth muscle occurs during hypertrophy induced by increasing vascular distending pressure. In addition, we also 96 describe changes found in the number and distribution ofactin and myosin filaments of hypertrophied vascular smooth muscle . These studies are being pursued to enable us to eventually distinguish the secondary effects of increased pressure on vascular smooth muscle from possible primary pathology of cell organelles that may cause hypertension. MATERIALS AND METHODSNew Zealand white male rabbits (1 .8-2 .7 kg) were anesthetized w...

The composition of normal, hypertrophied, or sodium-loaded rabbit portal anterior mesenteric vein and of normal and sodium-loaded guinea pig taenia coli smooth muscle was measured in cryosections with electron probe analysis, and the effects of wash with cold sodium-free (Lithium) solutions were determined. There was no significant difference in the cytoplasmic, nuclear, or mitochondrial concentrations of any of the measured elements (sodium, potassium, chloride, magnesium, calcium, phosphorus, sulfur) between hypertrophied, sham-operated, or control veins. The cytoplasmic potassium:sodium:chloride ratio in rabbit portal anterior mesenteric vein was 1:0.26:0.46, and the average sodium concentration (198 mmol/kg dry cytoplasmic weight) was nearly twice as high as estimated from ion flux measurements. The cytoplasmic sodium concentration of normal guinea pig taenia coli was 61 mmol/kg dry weight. The existence of a rapidly exchanging, relatively low affinity, and temperature-insensitive component of cytoplasmic sodium efflux was indicated by the reduction in cytoplasmic sodium after washout in cold, sodium-free (lithium or Tris-substituted) solutions. This reduction, by 62% in normal, 71% in sodium-loaded portal anterior mesenteric vein, and 36% in sodium-loaded guinea pig taenia coli smooth muscle, suggests that the lithium wash method can underestimate cell sodium. In sodium-loaded guinea pig taenia coli and portal anterior mesenteric vein smooth muscles, the cytoplasmic sodium analyzed in individual cells showed a bimodal distribution; in cryosections, the cells having the highest sodium and lowest potassium and phosphorus content also had a more electronlucent (light cell) appearance.